^TOP^
[Guidelines on treatment
of hypertension in the elderly, 1995--a tentative plan for comprehensive
research projects on aging and health-- Members of the Research Group
for "Guidelines on Treatment of Hypertension in the Elderly",
Comprehensive Research Projects on Aging and Health, the Ministry of
Health and Welfare of Japan]
Ogihara T, Hiwada K, Matsuoka H, Matsumoto M, Shimamoto K, Ouchi Y,
Abe I, Fujishima M, Morimoto S, Nakahashi T, Mikami H, Kohara K,
Takasaki M, Takizawa S, Kiyohara Y, Ibayashi S, Eto M, Ishimitsu T,
Nakamura T, Masusa A, Takagawa Y
Department of Geriatric Medicine, Osaka University Medical School.
Nippon Ronen Igakkai Zasshi 1996 Dec;33(12):945-75
We propose the following guidelines for treatment of hypertension in
the elderly. 1. Indications for Treatment.
1) Age: Lifestyle modification is recommended for patients aged 85
years and older. Antihypertensive therapy should be limited to patients
in whom the merit of the treatment is obvious.
2) Blood pressure: Systolic BP > 160 mmHg, diastolic BP > 90
approximately 10 mmHg. Systolic BP < age + 100 mmHg for those aged 70
years and older. Patients with mild hypertension (140-160/ 90-95 mmHg)
associated with cardiovascular disease should be considered for
antihypertensive drug therapy.
2. Goal of Therapy for BP: The goal BP in elderly patients is higher
than that in younger patients (BP reduction of 10-20 mmHg for systolic
BP and 5-10 mmHg for diastolic BP). In general, 140-160/< 90 mmHg is
recommended as the goal. However, lowering the BP below 150/85 should be
done with caution.
3. Rate of Lowering BP: Start with half the usual dose, observe at
the same dose for at least four weeks, and reach the target BP over two
months. Increasing the dose of antihypertensive drugs should be done
very slowly. 4. Lifestyle Modification:
1) Dietary modification:
(1) Reduction of sodium intake is highly effective in elderly
patients due to their high salt-sensitivity. NaCl intake of less than 10
g/day is recommended. Serum Na+ should be occasionally measured.
(2) Potassium supplementation is recommended, but with caution in
patients with renal insufficiency.
(3) Sufficient intake of calcium and magnesium is recommended.
(4) Reduce saturated fatty acids. Intake of fish is recommended.
(2) Regular physical activity: Recommended exercise for patients aged
60 years and older: peak heart rate 110/minute, for 30-40 minutes a day,
3-5 days a week.
(3) Weight reduction.
(4) Moderation of alcohol intake, smoking cessation. 5. Pharmacologic
Treatment:
1) Initial drug therapy. First choice: Long-acting (once or twice a
day) Ca antagonists or ACE inhibitors. Second choice: Thiazide diuretics
(combined with potassium-sparing diuretic).
2) Combination therapy.
(1) For patients without complications, either of the following is
recommended.
i) Ca antagoinst + ACE inhibitor,
ii) ACE inhibitor + Ca antagonist (or low-dose diuretics),
iii) diuretic + Ca antagonist (or ACE inhibitor), iv) beta-blockers,
alpha 1-blockers, alpha + beta blockers can be used according to the
patho-physiological state of the patient.
(2) For patients with complications. Drug(s) should be selected
according to each complication.
3) Relatively contraindicated drugs. beta-Blockers and alpha
1-blockers are relatively contraindicated in elderly patients with
hypertension in Japan. Centrally acting agents such as reserpine,
methyldopa and clonidine are also relatively contraindicated
beta-Blockers are contraindicated in patients with congestive heart
failure, arteriosclerosis obliterans, chronic obstructive pulmonary
disease, diabetes mellitus (or glucose intolerance), or bradycardia.
These conditions are often present in elderly subjects. Elderly subjects
are susceptible to alpha 1-blocker-induced orthostatic hypotension,
since their baroreceptor reflex is diminished. Orthostatic hypotension
may cause falls and bone fractures in the elderly.
^TOP^
Treatment of essential
hypertension with coenzyme Q10.
Langsjoen P; Langsjoen P; Willis R; Folkers K
Institute for Biomedical Research, University of Texas at Austin 78712,
USA.
Mol Aspects Med (England) 1994, 15 Suppl pS265-72
A total of 109 patients with symptomatic essential hypertension
presenting to a private cardiology practice were observed after the
addition of CoQ10 (average dose, 225 mg/day by mouth) to their existing
antihypertensive drug regimen. In 80 per cent of patients, the diagnosis
of essential hypertension was established for a year or more prior to
starting CoQ10 (average 9.2 years). Only one patient was dropped from
analysis due to noncompliance. The dosage of CoQ10 was not fixed and was
adjusted according to clinical response and blood CoQ10 levels. Our aim
was to attain blood levels greater than 2.0 micrograms/ml (average 3.02
micrograms/ml on CoQ10). Patients were followed closely with frequent
clinic visits to record blood pressure and clinical status and make
necessary adjustments in drug therapy. Echocardiograms were obtained at
baseline in 88% of patients and both at baseline and during treatment in
39% of patients. A definite and gradual improvement in functional status
was observed with the concomitant need to gradually decrease
antihypertensive drug therapy within the first one to six months.
Thereafter, clinical status and cardiovascular drug requirements
stabilized with a significantly improved systolic and diastolic blood
pressure. Overall New York Heart Association (NYHA) functional class
improved from a mean of 2.40 to 1.36 (P < 0.001) and 51% of patients
came completely off of between one and three antihypertensive drugs at
an average of 4.4 months after starting CoQ10. Only 3% of patients
required the addition of one antihypertensive drug. In the 9.4% of
patients with echocardiograms both before and during treatment, we
observed a highly significant improvement in left ventricular wall
thickness and diastolic function.
^TOP^
Coenzyme Q10 in essential
hypertension.
Digiesi V; Cantini F; Oradei A; Bisi G; Guarino GC; Brocchi A;
Bellandi F ; Mancini M; Littarru GP
Third institute of Clinical Medicine and Medical Therapy, University of
Florence Medical School, Italy.
Mol Aspects Med (England) 1994, 15 Suppl ps257-63
This study was undertaken to clarify the mechanism of the
antihypertensive effect of coenzyme Q10 (CoQ10). Twenty-six patients
with essential arterial hypertension were treated with oral CoQ10, 50 mg
twice daily for 10 weeks. Plasma CoQ10, serum total and high-density
lipoprotein (HDL) cholesterol, and blood pressure were determined in all
patients before and at the end of the 10-week period. At the end of the
treatment, systolic blood pressure (SBP) decreased from 164.5 +/- 3.1 to
146.7 +/- 4.1 mmHg and diastolic blood pressure (DBP) decreased from
98.1 +/- 1.7 to 86.1 +/- 1.3 mmHg (P < 0.001). Plasma CoQ10 values
increased from 0.64 +/- 0.1 microgram/ml to 1.61 +/- 0.3 micrograms/ml
(P < 0.02). Serum total cholesterol decreased from 222.9 +/- 13 mg/dl
to 213.3 +/- 12 mg/dl (P < 0.005) and serum HDL cholesterol increased
from 41.1 +/- 1.5 mg/dl to 43.1 +/- 1.5 mg/dl (P < 0.01). In a first
group of 10 patients serum sodium and potassium, plasma clinostatic and
orthostatic renin activity, urinary aldosterone, 24-hour sodium and
potassium were determined before and at the end of the 10-week period.
In five of these patients peripheral resistances were evaluated with
radionuclide angiocardiography. Total peripheral resistances were 2,283
+/- 88 dyne.s.cm-5 before treatment and 1,627 +/- 158 dyn.s.cm-5 after
treatment (P < 0.02). Plasma renin activity, serum and urinary sodium
and potassium, and urinary aldosterone did not change. In a second group
of 11 patients, plasma endothelin, electrocardiogram, two-dimensional
echocardiogram and 24-hour automatic blood pressure monitoring were
determined.
^TOP^
Usefulness of coenzyme Q10
in clinical cardiology: a long-term study.
Langsjoen H; Langsjoen P; Langsjoen P; Willis R; Folkers K
University of Texas Medical Branch, Galveston 77551, USA.
Mol Aspects Med (England) 1994, 15 Suppl ps165-75
Over an eight year period (1985-1993), we treated 424 patients with
various forms of cardiovascular disease by adding coenzyme Q10 (CoQ10)
to their medical regimens. Doses of CoQ10 ranged from 75 to 600 mg/day
by mouth (average 242 mg). Treatment was primarily guided by the
patient's clinical response. In many instances, CoQ10 levels were
employed with the aim of producing a whole blood level greater than or
equal to 2.10 micrograms/ml (average 2.92 micrograms/ml, n = 297).
Patients were followed for an average of 17.8 months, with a total
accumulation of 632 patient years. Eleven patients were omitted from
this study: 10 due to non-compliance and one who experienced nausea.
Eighteen deaths occurred during the study period with 10 attributable to
cardiac causes. Patients were divided into six diagnostic categories:
ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), primary
diastolic dysfunction (PDD), hypertension (HTN), mitral valve prolapse
(MVP) and valvular heart disease (VHD). For the entire group and for
each diagnostic category, we evaluated clinical response according to
the New York Heart Association (NYHA) functional scale, and found
significant improvement. Of 424 patients, 58 per cent improved by one
NYHA class, 28% by two classes and 1.2% by three classes. A
statistically significant improvement in myocardial function was
documented using the following echocardiographic parameters: left
ventricular wall thickness, mitral valve inflow slope and fractional
shortening. Before treatment with CoQ10, most patients were taking from
one to five cardiac medications. During this study, overall medication
requirements dropped considerably: 43% stopped between one and three
drugs. Only 6% of the patients required the addition of one drug. No
apparent side effects from CoQ10 treatment were noted other than a
single case of transient nausea. In conclusion, CoQ10 is a safe and
effective adjunctive treatment for a broad range of cardiovascular
diseases, producing gratifying clinical responses while easing the
medical and financial burden of multidrug therapy.
^TOP^
Influence of coenzyme Q-10
on the hypotensive effects of enalapril and nitrendipine in
spontaneously hypertensive rats.
Danysz A; Oledzka K; Bukowska-Kiliszek M
Department of Pharmacology, Pharmaceutical Research Institute Rydygiera,
Warszawa, Poland.
Pol J Pharmacol (Poland) Sep-Oct 1994, 46 (5) p457-61
Administration of coenzyme Q-10 (10 mg/kg) once a day for 4 weeks
decreased the arterial blood pressure in SHR's. Enalapril and
nitrendipine administered in a single dose caused significant decrease
of blood pressure. Application of enalapril and nitrendipine to rats
chronically pretreated with coenzyme Q-10 revealed, that the maximal
hypotensive effect was not greater, but it lasted much (ca. 2-times)
longer. Independently of mechanism of this interaction it may be
suggested that the chronic administration of coenzyme Q-10 would create
the possibility of significant decrease of the frequency of some
antihypertensive drug administration.
^TOP^
Isolated diastolic
dysfunction of the myocardium and its response to CoQ10 treatment.
Langsjoen PH; Langsjoen PH; Folkers K
Clin Investig (Germany) 1993, 71 (8 Suppl) pS140-4
Symptoms of fatigue and activity impairment, atypical precordial
pain, and cardiac arrhythmia frequently precede by years the development
of congestive heart failure. Of 115 patients with these symptoms, 60
were diagnosed as having hypertensive cardiovascular disease, 27 mitral
valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms
are common with diastolic dysfunction, and diastolic function is energy
dependent. All patients had blood pressure, clinical status, coenzyme
Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic
function, systolic function, and myocardial thickness recorded before
and after CoQ10 replacement. At control, 63 patients were functional
class III and 54 class II; all showed diastolic dysfunction; the mean
CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed
significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated
blood pressure readings in hypertensive disease, mitral valve prolapse
and chronic fatigue syndrome respectively. Except for higher blood
pressure levels and more myocardial thickening in the hypertensive
patients, there was little difference between the three groups. CoQ10
administration resulted in improvement in all; reduction in high blood
pressure in 80%, and improvement in diastolic function in all patients
with follow-up echocardiograms to date; a reduction in myocardial
thickness in 53% of hypertensives and 36% of the combined prolapse and
fatigue syndrome groups; and a reduced fractional shortening in those
high at control and an increase in those initially low.
^TOP^
Effect of coenzyme Q10 on
structural alterations in the renal membrane of stroke-prone
spontaneously hypertensive rats.
Okamoto H; Kawaguchi H; Togashi H; Minami M; Saito H; Yasuda H
Department of Cardiovascular, Hokkaido University, Japan.
Biochem Med Metab Biol (United States) Apr 1991, 45 (2) p216-26
To test the hypothesis that structural abnormalities exist in the
kidney membrane of spontaneously hypertensive rats, we examined the
effect of long-term administration of coenzyme Q10 on membrane lipid
alterations in the kidney of stroke-prone spontaneously hypertensive
rats (SHRSP). As compared with normotensive Wistar-Kyoto rats, renal
membrane phospholipids, especially phosphatidylcholine and
phosphatidylethanolamine, decreased and renal phospholipase A2 activity
was enhanced with age in untreated SHRSP. Treatment with coenzyme Q10
attenuated the elevation of blood pressure, the membranous phospholipid
degradation, and the enhanced phospholipase A2 activity. These results
suggest that one factor contributing to the progress of hypertension is
a structural membrane abnormality that alters the physical and
functional properties of the cell membrane, and coenzyme Q10 might
protect the renal membrane from damage due to hypertension in SHRSP.
^TOP^
Co-enzyme Q10: a new drug
for cardiovascular disease.
Greenberg S; Frishman WH
Department of Medicine, Mt. Sinai Hospital and Medical Center, New York,
New York
J Clin Pharmacol (United States) Jul 1990, 30 (7) p596-608
Co-enzyme Q10 (ubiquinone) is a naturally occurring substance which
has properties potentially beneficial for preventing cellular damage
during myocardial ischemia and reperfusion. It plays a role in oxidative
phosphorylation and has membrane stabilizing activity. The substance has
been used in oral form to treat various cardiovascular disorders
including angina pectoris, hypertension, and congestive heart failure.
Its clinical importance is now being established in clinical trails
worldwide.
^TOP^
Coenzyme Q10: a new drug
for myocardial ischemia?
Greenberg SM; Frishman WH
Department of Medicine, Mt. Sinai Hospital and Medical School, New York,
New York
Med Clin North Am (United States) Jan 1988, 72 (1) p243-58
A biochemical rationale for using CoQ in treating certain
cardiovascular diseases has been established. CoQ subserves an
endogenous function as an essential cofactor in several metabolic
pathways, particularly oxidative respiration. As an exogenous source in
supraphysiologic doses, CoQ may have pharmacologic effects that are
beneficial to tissues rendered ischemic and then reperfused. Its
mechanism of action appears to be that of a free radical scavenger
and/or direct membrane stabilizer. Initial clinical studies performed
abroad and in the United States indicate that CoQ may be effective in
treating certain patients with ischemic heart disease, congestive heart
failure, toxin-induced cardiotoxicity, and possibly hypertension. The
most intriguing property of CoQ is its potential to protect and preserve
ischemic myocardium during surgery. Currently, CoQ is still considered
an experimental agent and only further studies will determine whether it
will be useful therapy for human cardiovascular disease states.
^TOP^
Bioenergetics in clinical
medicine. XVI. Reduction of hypertension in patients by therapy with
coenzyme Q10.
Folkers K; Drzewoski J; Richardson PC; Ellis J; Shizukuishi S; Baker
L
Res Commun Chem Pathol Pharmacol (United States) Jan 1981, 31 (1)
p129-40
Six untreated hypertensive patients and ten on therapy, but having
elevated blood pressures, were treated with coenzyme Q10(CoQ10); 14/16
patients showed reductions (p less than 0.05-less than 0.001) in
systolic pressures; 11/16 showed reductions (p less than 0.05-less than
0.001) in diastolic pressure; 9/10 showed reductions of elevated
pressures to a normal range. By impedance cardiography and
electrocardiography, there were no changes in cardiac outputs, stroke
volumes and Heather Indices except for a few patients with changes of
doubtful biological significance. 3/16 patients had exceptionally low
basal specific activities of the succinate dehydrogenase-coenzyme Q10
reductase in blood which increased to a normal range on treatment. A
greater deficiency of CoQ10 in the vascular system than in blood is
likely. We consider that (1) the mechanism of reduction of elevated
blood pressures by CoQ10 is based upon normalization or autoregulation
of peripheral resistance rather than cardiac regulation, and (2) that
the therapeutic activity of CoQ10 is not pharmacodynamic, but results
from a translational increase in levels of CoQ10-enzymes in vascular
tissue during ca. 4-12 weeks.
^TOP^
Bioenergetics in clinical
medicine. VIII. Adminstration of coenzyme Q10 to patients with essential
hypertension.
Yamagami T; Shibata N; Folkers K
Res Commun Chem Pathol Pharmacol (United States) Aug 1976, 14 (4) p721-7
Coenzyme Q10 has been administered to five patients having essential
hypertension and deficiencies of activity of succinate
dehydrogenase-co-enzyme Q10 reductase in leucocyte preparations ranging
from 20-40%. For a 74-year old male, the systolic pressure was reduced
(p less than 0.001), the diastolic pressure was reduced (p less than
0.05), the specific activity of the coenzyme Q10-enzyme was increased (p
less than 0.001), and the deficiency of coenzyme Q10 activity was
negated (p less than 0.01). Four patients receiving CoQ10 for 3-5 months
showed reductions (p less than 0.05 to p less than 0.001) of diastolic
pressure, and 3 of these 4 showed reductions (p less than 0.05 to p less
than 0.01) of diastolic pressure. Initial deficiencies of enzyme
activity were reduced (p less than 0.01 to 0.05) in two patients. Three
other patients did not show the high level of deficiency on treatment as
initially observed. These effects of CoQ10 on the reduction of systolic
and diastolic blood pressures, increase in CoQ10-enzyme activity, and
reduction of CoQ10-deficiency are presumably due to improved
bioenergetics through correction of a deficiency of coenzyme Q10.
^TOP^
Bioenergetics in clinical
medicine. III. Inhibition of coenzyme Q10-enzymes by clinically used
anti-hypertensive drugs.
Kishi H; Kishi T; Folkers K
Res Commun Chem Pathol Pharmacol (United States) Nov 1975, 12 (3)
p533-40
Background data revealed that some American and Japanese patients
with essential hypertension, including many who were not being treated
with any anti-hypertensive drug, had a deficiency of coenzyme Q10. Eight
clinically used anti-hypertensive drugs have now been tested for
inhibition of two mitochondrial coenzyme Q10-enzymes of heart tissue,
succinoxidase and NADH-oxidase. Diazoxide and propranolol significantly
inhibited the CoQ10-succinoxidase and CoQ10-NADH-oxidase, respectively.
Metoprolol did not inhibit succinoxidase, and was one-fourth as active
as propranolol for inhibition of NADH-oxidase. Hydrochlorothiazide,
hydralazine, ans clonidine also inhibited CoQ10-NADH-oxidase. Reserpine
did not inhibit either CoQ10-enzyme, and methyldopa was a very eak
inhibitor of succinoxidase. The internationally recognized clinical
side-effects of propranolol may be due, in part, to inhibition of
CoQ10-enzymes which are indispensable in the bioenergetics of cardiac
function. A pre-existing deficiency of coenzyme Q10 in the myocardium of
hypertensive patients could be augmented by subsequent treatment with
propranolol, possibly to the "life-threatening" state
described by others.
^TOP^
Bioenergetics in clinical
medicine. Studies on coenzyme Q10 and essential hypertension.
Yamagami T; Shibata N; Folkers K
Res Commun Chem Pathol Pharmacol (United States) Jun 1975, 11 (2)
p273-88
The specific activities (S.A.) of the succinate
dehydrogenase-coenzyme Q10 (CoQ10) reductase of a control group of 65
Japanese adults and 59 patients having essential hypertension were
determined. The mean S.A. of the hypertensive group was significantly
lower (p less than 0.001) and the mean % deficiency of enzyme activity
was significantly higher (p less than 0.001) than the values for the
control group. These data on Japanese in Osaka agree with data on
Americans in Dallas. Some patients showed no CoQ10-deficiency, and
others showed definite deficiencies. Emphasizing the CoQ10-enzyme for
patient selection, CoQ10 was administered to hypertensive patients. Four
individuals showed significant but partial reductions of blood pressure.
Monitoring the CoQ10-enzyme before, during, and after administration of
CoQ10 indicated responses. The maintenance of high blood pressure could
be primarily due to contraction of the arterial wall. Contraction or
relaxation of an arterial wall is dependent upon bioenergetics, which
also provide the energy for biosynthesis of angiotensin II, renin,
aldosterone, and the energy for sodium and potassium transport. A
clinical benefit from administration of CoQ10 to patients with essential
hypertension could be based upon correcting a deficiency in
bioenergetics, and point to possible combination treatments with a form
of CoQ and anti-hypertensive drugs.
^TOP^
[Garlic (Allium
sativum)--a potent medicinal plant]
Resch KL; Ernst E
Postgraduate Medical School, University of Exeter, UK.
Fortschr Med (Germany) Jul 20 1995, 113 (20-21) p311-5
A good deal of evidence suggests beneficial effects of the regular
dietary intake of garlic on mild hypertension and hyperlipidemia. Garlic
seems to have anti-microbial and immunostimulating properties, enhance
fibrinolytic activity, and exert favorable effects on platelet
aggregation and adhesion. Standardised preparations guarantee exact
dosing and minimize the problem of the strong odour of raw garlic. Thus,
a traditional folk remedy has established its usefulness for many
patients with less severe forms of cardiovascular disease as a medical
drug with very few side effects. The available evidence gives rise to
the hope that the list of indications may even be considerably extended
in the future. (43 Refs.)
^TOP^
A meta-analysis of the
effect of garlic on blood pressure.
Silagy CA; Neil HA
Department of General Practice, Flinders University of South Australia,
Adelaide.
J Hypertens (England) Apr 1994, 12 (4) p463-8
OBJECTIVE: To undertake a systematic review, including meta-analysis,
of published and unpublished randomized controlled trials of garlic
preparations to determine the effect of garlic on blood pressure
relative to placebo and other antihypertensive agents.
DATA IDENTIFICATION: Studies were identified by a search of Medline
and the Alternative Medicine electronic databases, from references
listed in primary and review articles, and through direct contact with
garlic manufacturers.
STUDY SELECTION: Only randomized controlled trials of garlic
preparations that were at least 4 weeks in duration were deemed eligible
for inclusion in the review.
DATA EXTRACTION: Data were extracted from the published reports by
the two authors independently, with disagreements resolved by
discussion.
RESULTS: Eight trials were identified (all using the same dried
garlic powder preparation (Kwai) with data from 415 subjects included in
the analyses. Only three of the trials were specifically conducted in
hypertensive subjects, and many had other methodological shortcomings.
Of the seven trials that compared the effect of garlic with that of
placebo, three showed a significant reduction in systolic blood pressure
(SBP) and four in diastolic blood pressure (DBP). The overall pooled
mean difference in the absolute change (from baseline to final
measurement) of SBP was greater in the subjects who were treated with
garlic then in those treated with placebo. For DBP the corresponding
reduction in the garlic-treated subjects was slightly smaller.
CONCLUSIONS: The results suggest that this garlic powder preparation
may be of some clinical use in subjects with mild hypertension. However,
there is still insufficient evidence to recommend it is a routine
clinical therapy for the treatment of hypertensive subjects.
More-rigorously designed and analysed trials are needed.
^TOP^
Patient preferences for
novel therapy: an N-of-1 trial of garlic in the treatment for
hypertension.
Estrada CA; Young MJ
Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan
48202.
J Gen Intern Med (United States) Nov 1993, 8 (11) p619-21
The authors used the N-of-1 clinical trial methodology to obtain
insights about a patient's preference for garlic for the management of
his hypertension. The 61-year-old man received garlic, 500 mg by mouth
three times a day (3 weeks), or identical placebo (3 weeks) in three
treatment pairs. While the patient was taking garlic the mean systolic
blood pressure decreased by 2 mm Hg (95% confidence interval 0.4 to 4.7,
p < 0.05), and the diastolic blood pressure decreased by 2.4 mm Hg
(95% confidence interval 0.4 to 4, p < 0.025). The treatment effect
of garlic was small, but the patient believed continuing garlic for the
management of his hypertension was justified.
^TOP^
Can garlic lower blood
pressure? A pilot study.
McMahon FG; Vargas R
Clinical Research Center, New Orleans, LA 70112.
Pharmacotherapy (United States) Jul-Aug 1993, 13 (4) p406-7
A popular garlic preparation containing 1.3% allicin at a large dose
(2400 mg) was evaluated in this open-label study in nine patients with
rather severe hypertension (diastolic blood pressure > or = 115 mm
Hg). Sitting blood pressure fell 7/16 (+/- 3/2 SD) mm Hg at peak effect
approximately 5 hours after the dose, with a significant decrease in
diastolic blood pressure (p < 0.05) from 5-14 hours after the dose.
No significant side effects were reported. Our results indicate that
this garlic preparation can reduce blood pressure. Further controlled
studies are needed, particularly with more conventional doses (e.g.,
< or = 900 mg/day), in patients with mild to moderate hypertension
and under placebo-controlled, double-blind conditions.
^TOP^
Hypertension and
hyperlipidaemia: garlic helps in mild cases.
Auer W; Eiber A; Hertkorn E; Hoehfeld E; Koehrle U; Lorenz A; Mader
F; Merx W; Otto G; Schmid-Otto B; et al
Incorporated Society, Nittendorf, West Germany.
Br J Clin Pract Symp Suppl (England) Aug 1990, 69 p3-6
Forty-seven non-hospitalised patients with mild hypertension took
part in a randomised, placebo-controlled, double-blind trial conducted
by 11 general practitioners. The patients who were admitted had
diastolic blood pressures between 95 and 104 mmHg after a two-week
acclimatization phase. The patients then took either a preparation of
garlic powder (Kwai) or a placebo of identical appearance for 12 weeks.
Blood pressure and plasma lipids were monitored during treatment after
four, eight and 12 weeks. Significant differences between the placebo
and the drug group were found during the course of therapy. For example,
the supine diastolic blood pressure in the group having garlic treatment
fell from 102 to 91 mmHg after eight weeks (p less than 0.05) and to 89
mmHg after 12 weeks (p less than 0.01). The serum cholesterol and
triglycerides were also significantly reduced after eight and 12 weeks
of treatment. In the placebo group, on the other hand, no significant
changes occurred.
^TOP^
Defective renal adenylate
cyclase response to prostaglandin E2 in spontaneously hypertensive rats.
Umemura S; Smyth DD; Pettinger WA
J Hypertens (England) Apr 1985, 3 (2) p159-65
We activated three known components of the adenylate cyclase system
in renal membranes from spontaneously hypertensive (SHR) and
Wistar-Kyoto (WKY) rats. The basal adenylate cyclase activity and
responses to plasma membrane receptor activation by parathyroid hormone,
isoproterenol and vasopressin were not different between the two
strains. The response to prostaglandin E2 (PGE2), however, was less in
the SHR than in the WKY at five, (P less than 0.05), 12 (P less than
0.01) and 16 (P less than 0.01) weeks of age. Activation of either the
guanosine-5'-triphosphate (GTP) binding regulatory protein (N) with
sodium fluoride (NaF) and guanyl-5'-yl-imidodiphosphate [Gpp(NH)p], or
the catalytic unit with manganese chloride (MnCl2) or forskolin were not
different between the two groups. When the medullary and cortical plasma
membrane adenylate cyclase responses were studied separately, the
observed decreased response to PGE2 (of SHR) was found to be entirely in
the cortex. Also, the NaF response was reduced in the cortical region of
the 12-week-old rats, a finding suggesting a possibility of a post
receptor defect. These results show that there is a defective renal
adenylate cyclase response specific to prostaglandin E2 in SHR. This
defect could be related to the development of hypertension, by changing
the natriuretic and/or renal vasodilating effects
^TOP^
Renal response to
L-arginine in salt-sensitive patients with essential hypertension.
Higashi Y; Oshima T; Watanabe M; Matsuura H; Kajiyama G
First Department of Internal Medicine, Hiroshima University School of
Medicine, Japan.
Hypertension (United States) Mar 1996, 27 (3 Pt 2) p643-8
This study examined whether disturbances in nitric oxide formation
contribute to renal dysfunction in salt-sensitive essential hypertensive
patients. We evaluated the effects of intravenous administration of
L-arginine (500 mg/kg given over 30 minutes) on systemic and renal
hemodynamics in 23 patients with mild essential hypertension during 1
week of a low NaCl diet (50 mmol/d) followed by 1 week of a high NaCl
diet (340 mmol/d). Patients were classified as salt sensitive (n=10) or
salt resistant (n=13) based on salt-induced changes in their blood
pressures. Salt loading increased renal vascular resistance but not
renal plasma flow in salt-sensitive patients. The L-arginine-induced
renovascular relaxation was significantly reduced by a high NaCl diet
(renal vascular resistance: low NaCl -12.4 +/- 2.3% versus high NaCl
-7.1 +/- 1.8%, P < .001) in salt-sensitive patients, whereas it was
unchanged in salt-resistant patients. The increase in plasma cGMP in
response to L-arginine was also reduced by a high NaCl diet in the
salt-sensitive patients (low NaCl 49 +/- 7% versus high NaCl 36 +/- 8%,
P < .05) but not in the salt-resistant patients (low NaCl 51 +/- 6%
versus high NaCl 58 +/- 6%). These findings suggest that NaCl loading in
salt-sensitive patients with mild essential hypertension reduces the
ability of L-arginine to produce nitric oxide in the endothelium of the
renal vasculature.
^TOP^
L-arginine restores
dilator responses of the basilar artery to acetylcholine during chronic
hypertension.
Kitazono T; Faraci FM; Heistad DD
Department of Internal Medicine, Cardiovascular Center, University of
Iowa College of Medicine, Iowa City 52242, USA.
Hypertension (United States) Apr 1996, 27 (4) p893-6
The objective of this study was to test the hypothesis that
administration of L-arginine, a substrate for nitric oxide synthase,
restores acetylcholine-induced dilatation of the basilar artery in
chronically hypertensive rats. Basilar artery diameter was measured
through a cranial window in anesthesized stroke-prone spontaneously
hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) aged
6 to 7 months (adult) and 12 months (older adult). Under control
conditions, baseline basilar artery diameter was smaller in SHRSP
(adult, 239 +/- 30 micron; older adult, 198 +/- 13 micron) (mean +/- SE)
than in WKY (adult, 261 +/- 10 micron; older adult, 259 +/- 7 micron) (P
<.05 versus SHRSP). Topical application of acetylcholine (10(-5)
mol/L) produced dilatation of the basilar artery in WKY, which was
impaired in both adult and older SHRSP (P <.05). Topical L-arginine
(10(-3) mol/L for 30 minutes) did not affect responses to acetylcholine
in adult SHRSP but enhanced vasodilatation in response to acetylcholine
(10(-5) mol/L) in older SHRSP without affecting responses to sodium
nitroprusside. In contrast, D-arginine did not affect
acetylcholine-induced vasodilatation in older SHRSP. These results
suggest that impaired dilatation of the basilar artery in response to
acetylcholine in older SHRSP is restored toward normal by L-arginine, a
substrate for nitric oxide synthase.
^TOP^
Vitamin-C deficiency and
low linolenate intake associated with elevated blood pressure: the
Kuopio Ischaemic Heart Disease Risk Factor Study.
Salonen JT; Salonen R; Ihanainen M; Parviainen M; Seppanen R;
Seppanen K; Rauramaa R
Department of Community Health, University of Kuopio, Finland.
J Hypertens Suppl (England) Dec 1987, 5 (5) pS521-4
We investigated the association of dietary fatty acids and plasma
antioxidative vitamins with blood pressure in 722 eastern Finnish men
aged 54 years, examined in the Kuopio Ischaemic Heart Disease Risk
Factor Study in 1984-1986, who had no known hypertension nor any
cerebrovascular disease. Allowing for the major anthropometric, dietary,
medical and psychological determinants of blood pressure in a
multivariate regression analysis, plasma ascorbic acid concentration had
a moderate, independent inverse association (P less than 0.0001) and the
estimated dietary intake of linolenic acid an inverse (P = 0.026)
independent association with mean resting blood pressure. The marked
elevation of blood pressure at the lowest levels of plasma Vitamin-C
concentration supports the hypothesis of the role of antioxidants in the
aetiology of hypertension.
^TOP^
Regulation of blood
pressure by nitroxidergic nerve.
Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu,
Japan.
J Diabetes Complications (United States) Oct-Dec 1995, 9 (4) p200-2
We discovered vasodilator innervation first in canine cerebral
arteries, in which nitric oxide (NO) acts as a neurotransmitter; thus,
the nerve is called nitroxidergic. Then, reciprocal innervation of
noradrenergic and nitroxidergic nerves in canine peripheral arteries was
determined; adrenergic nerve-mediated vasoconstriction is predominant
over vasodilatation mediated by NO derived from the nerve. In
anesthetized dogs, hypertension induced by NO synthase inhibitors is
suppressed by hexamethonium. It is hypothesized that impairment of
nitroxidergic nerve function by NO synthase inhibition is mainly
involved in the genesis of hypertension.
^TOP^
[Endothelial function and
arterial hypertension]
Taddei S; Virdis A; Ghiadoni L; Salvetti A
Cattedra di Medicina Interna, Universita degli Studi di Pisa.
Ann Ital Med Int (Italy) Oct 1995, 10 Suppl p85S-90S
In normotensive humans, the endothelium modulates vascular tone
mainly by the production of nitric oxide. In human essential
hypertension the basal release of nitric oxide is reduced and forearm
vasodilation to the endothelium-dependent agonists acetylcholine or
bradykinin is blunted. Defective basal release of nitric oxide seems to
be secondary to blood pressure increase while impaired agonist-evoked
endothelium-dependent vasodilation is probably a primary phenomenon.
This latter endothelial dysfunction seems to be caused by the
simultaneous presence of an alteration in the L-arginine-nitric oxide
pathway and the production of constrictor prostanoids. Defective nitric
oxide production is already detectable in normotensive offspring of
hypertensive patients and young essential hypertensives. In contrast,
vasoconstrictor prostanoid production seems to be associated with aging.
In essential hypertensive patients, although only scanty data are
available, chronic effective pharmacological treatment seems to restore
impaired basal production of nitric oxide but does not improve vascular
response to endothelial agonists. (34 Refs.)
^TOP^
Contrasting effect of
antihypertensive treatment on the renal response to L-arginine.
Mimran A; Ribstein J; DuCailar G
Department of Medicine, Centre Hospitalier Universitaire, Montpellier,
France.
Hypertension (United States) Dec 1995, 26 (6 Pt 1) p937-41
We assessed the renal hemodynamic response to L-arginine infusion (30
g within 60 minutes) in normotensive subjects, patients with
never-treated essential hypertension, and hypertensive patients
controlled by long-term (more than 2 years) treatment with or without an
angiotensin-converting enzyme inhibitor. The renal vasodilator response
to L-arginine observed in normotensive subjects (15 +/- 4% increase in
effective renal plasma flow) was abolished in untreated hypertensive
patients and restored only in the group treated by
angiotensin-converting enzyme inhibition. In the whole population a
positive correlation between the change in effective renal plasma flow
and the change in urinary cGMP was obtained. It is suggested that
abnormalities of the renal nitric oxide pathway not corrected by
increased availability of L-arginine and reversible only on long-term
treatment by angiotensin-converting enzyme inhibition may underlie the
abnormal renal resistance observed in essential hypertension.
^TOP^
Prospective study of
nutritional factors, blood pressure, and hypertension among US women.
Ascherio A; Hennekens C; Willett WC; Sacks F; Rosner B; Manson J;
Witteman J; Stampfer MJ
Department of Nutrition, Harvard School of Public Health, Boston, Mass
02115, USA.
Hypertension (United States) May 1996, 27 (5) p1065-72
We examined prospectively the relation of nutritional factors with
hypertension and blood pressure levels among 41,541 predominantly white
US female nurses, aged 38 to 63 years, who completed a detailed
semiquantitative food frequency questionnaire in 1984 and were without
diagnosed hypertension, cancer, or cardiovascular disease. During 4
years of follow-up, from 1984 to 1988, 2,526 women reported a diagnosis
of hypertension. Age, relative weight, and alcohol consumption were the
strongest predictors for the development of hypertension. Dietary
calcium, magnesium, potassium, and fiber were not significantly
associated with risk of hypertension, after adjusting for age, body mass
index, alcohol, and energy intake. Among women who did not report
hypertension during the follow-up period, calcium, magnesium, potassium,
and fiber were each significantly inversely associated with
self-reported systolic and diastolic pressures, after adjusting for age,
body mass index, alcohol consumption, and energy intake. When the four
nutrients were added simultaneously to the regression model, only fiber
and magnesium intakes retained significant inverse associations with
systolic and diastolic pressures. In analyses of food groups, intakes of
fruit and vegetables were inversely associated with systolic and
diastolic pressures, and intakes of cereals and meat were directly
associated with systolic pressure. These results support hypotheses that
age, body weight, and alcohol consumption are strong determinants of
risk of hypertension in middle-aged women. They are compatible with the
possibilities that magnesium and fiber as well as a diet richer in
fruits and vegetables may reduce blood pressure levels.
^TOP^
[Overview--suppression
effect of essential trace elements on arteriosclerotic development and
it's mechanism]
Saito N
Nippon Rinsho (Japan) Jan 1996, 54 (1) p59-66
It is known that the peroxidation of LDL is a trigger for developing
arteriosclerosis. The oxidized LDL is produced by either oxidative
stress or a few oxidant. Selenium decreased in serum and some organs of
stroke-prone spontaneously hypertensive rats (SHRSP), which is a
cofactor of glutamine peroxidase. Serum magnesium decreased in patients
with diabetes mellitus, with ischemic heart disease, with essential
hypertension and with cerebral vascular lesions. Calcium to magnesium
ratio was higher in some organs of SHRSP as compared to Wistar Kyoto
rats (WKY). These changes accelerated vascular lesions in SHRSP.
^TOP^
[Interrelationship
between dietary intake of minerals and prevalence of hypertension]
Davydenko NV; Smirnova IP; Kvasha EA; Gorbas' IM; Koblianskaia AV
Vopr Pitan (Russia) 1995, (6) p17-9
1556 of men living in Kiev aged 20-59 years were examined to evaluate
interrelationship between the dietary intakes of Ca, Mg, P, Fe, Cu, Zn
and level of arterial blood pressure (AP). Dietary intake was studied by
24-h recall methodology. Systolic AP > 160 mm Hg and/or diastolic AP
> 90 mm Hg were referred as arterial hypertension (AH). It was shown
that high dietary intakes of Ca or Zn were related with the higher rate
of AH. At low level of dietary intake of Mg, Cu or P the prevalence of
AH was seen in 1.8-2 times more often than at high level of intake of
these micronutrients. Mean systolic AP had trend to increasing and
diastolic AP was significant higher at low level of dietary intake of P.
Correction of dietary intake of microelements should be used in
preventive measures of AH.
^TOP^
Potassium depletion and
salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium,
and phosphate excretions.
Wu X; Ackermann U; Sonnenberg H
Department of Physiology, University of Toronto, Ontario, Canada.
Clin Exp Hypertens 1995 Aug;17(6):989-1008
Weanling male inbred Dahl rats (Jr salt-sensitive (S) and
salt-resistant (R) strains) were placed on high (4%, HK) and low (0.2%,
LK) potassium diets for 4 weeks. Both diets contained 8% sodium
chloride, 2.5% calcium, 0.8% magnesium, and 2.0% phosphorous. Balance
studies were carried out during the final week on the diets. Mean
arterial blood pressure was determined, and dietary intake and urinary
output of water, sodium, chloride, potassium, calcium, magnesium, and
phosphate were monitored daily during this period. The data show that
blood pressures of S rats were significantly higher than those of R rats
on both HK and LK diets; however, reduced dietary potassium was
associated with increased blood pressure in both strains. Urinary
excretions of calcium and magnesium were higher, and urinary phosphate
excretion was lower, in S compared to R rats. Decreased potassium intake
was associated with increased excretion of calcium, magnesium and
phosphate in both strains. The changes in calcium and magnesium
excretion were significantly correlated to blood pressure across strains
and diets. We conclude that the effects of a high salt diet on
increasing blood pressure can be potentiated by lack of potassium, even
in previously salt-resistant rats. Increased blood pressure is
associated with increased divalent cation excretion. It is not yet known
whether this is a cause-and-effect relationship.
^TOP^
Consequences of magnesium
deficiency on the enhancement of stress reactions; preventive and
therapeutic implications (a review).
Seelig MS
Department of Nutrition, School of Public Health, University of North
Carolina, Chapel Hill.
J Am Coll Nutr (United States) Oct 1994, 13 (5) p429-46
Stress intensifies release of catecholamines and corticosteroids that
increase survival of normal animals when their lives are threatened.
When magnesium (Mg) deficiency exists, stress paradoxically increases
risk of cardiovascular damage including hypertension, cerebrovascular
and coronary constriction and occlusion, arrhythmias and sudden cardiac
death (SCD). In affluent societies, severe dietary Mg deficiency is
uncommon, but dietary imbalances such as high intakes of fat and/or
calcium (Ca) can intensify Mg inadequacy, especially under conditions of
stress. Adrenergic stimulation of lipolysis can intensify its deficiency
by complexing Mg with liberated fatty acids (FA), A low Mg/Ca ratio
increases release of catecholamines, which lowers tissue (i.e.
myocardial) Mg levels. It also favors excess release or formation of
factors (derived both from FA metabolism and the endothelium), that are
vasoconstrictive and platelet aggregating; a high Ca/Mg ratio also
directly favors blood coagulation, which is also favored by excess fat
and its mobilization during adrenergic lipolysis. Auto-oxidation of
catecholamines yields free radicals, which explains the enhancement of
the protective effect of Mg by anti-oxidant nutrients against cardiac
damage caused by beta-catecholamines. Thus, stress, whether physical
(i.e. exertion, heat, cold, trauma--accidental or surgical, burns), or
emotional (i.e. pain, anxiety, excitement or depression) and dyspnea as
in asthma increases need for Mg. Genetic differences in Mg utilization
may account for differences in vulnerability to Mg deficiency and
differences in body responses to stress.
^TOP^
Relationship of magnesium
intake and other dietary factors to blood pressure: the Honolulu heart
study.
Joffres MR; Reed DM; Yano K
Am J Clin Nutr (United States) Feb 1987, 45 (2) p469-75
Associations between blood pressure and intakes of 61 dietary
variables assessed by 24-h recall method were investigated in 615 men of
Japanese ancestry living in Hawaii who had no history of cardiovascular
disease or treated hypertension. Magnesium, calcium, phosphorus,
potassium, fiber, vegetable protein, starch, Vitamin-C, and vitamin D
intakes were significant variables that showed inverse associations with
blood pressure in univariate and a multivariate analyses. Magnesium had
the strongest association with blood pressure, which supports recent
interest in its relation to blood pressure. Nevertheless, it was not
possible to separate the effect of magnesium from that of other
variables because of the problem of high intercorrelation among many
nutrients. While recommendations based upon cross-sectional studies must
be viewed cautiously, these results suggest that foods such as
vegetables, fruits, whole grains, and low-fat dairy items are major
sources of nutrients that may be protective against hypertension.
^TOP^
[Role of electrolytes in
the development and maintenance of hypertension]
Fujita T; Ando K
Fourth Department of Internal Medicine, University of Tokyo School of
Medicine, Japan.
Nippon Naibunpi Gakkai Zasshi (Japan) May 20 1994, 70 (4) p423-30
Sodium (Na) intake is one of the important environmental factors
influencing the development and maintenance of high blood pressure (BP).
Patients with essential hypertension can be divided into two groups:
"salt-sensitive" and "non-salt-sensitive", according
to BP response to salt loading, suggesting the heterogeneity of salt
sensitivity of BP. Salt-sensitive patients had greater increases in BP
by salt loading, associated with greater Na retention. Although the
precise mechanism for impaired renal Na handling in salt-sensitive
patients is still unknown, the sympathetic nervous system in the kidney
may play an important role in the decreased renal function of Na
excretion and the increased salt sensitivity. Moreover, there are
several pieces of evidence indicating that increased renal sympathetic
nerve activity is intimately related to the abnormal central
noradrenergic systems. In addition, the renin-angiotensin system,
insulin, and so on, may modulate salt sensitivity of BP. Some ions
influence the hypertensinogenic effect of Na: Chloride ion facilitates
it, while potassium, calcium and magnesium antagonize it. Moreover,
obesity and a stressful environment increase salt sensitivity of BP.
^TOP^
Effect of dietary
magnesium supplementation on intralymphocytic free calcium and magnesium
in stroke-prone spontaneously hypertensive rats.
Adachi M; Nara Y; Mano M; Yamori Y
Department of Pathology, Shimane Medical University, Izumo, Japan.
Clin Exp Hypertens (United States) May 1994, 16 (3) p317-26
The effects of dietary magnesium (Mg) supplementation on
intralymphocytic free Ca2+ ([Ca2+]i) and Mg2+ ([Mg2+]i) were examined in
the stroke-prone spontaneously hypertensive rats (SHRSP) at the age of
10 weeks. After 40 day Mg supplementation (0.8% Mg in the diet),
systolic blood pressure (SBP) was significantly lower in Mg supplemented
group (Mg group) than the control group (0.2% Mg). [Ca2+]i was
significantly lower and [Mg2+]i was significantly higher in Mg group
than in the control group. Further, [Ca2+]i was positively and [Mg2+]i
was negatively correlated with SBP. These results suggest that dietary
Mg supplementation modifies [Ca2+]i and [Mg2+]i, and modulates the
development of hypertension.
^TOP^
Vasorelaxant properties
of n-3 polyunsaturated fatty acids in aortas from spontaneously
hypertensive and normotensive rats.
Engler MB; Engler MM; Ursell PC
University of California, Department of Physiological Nursing, San
Francisco, 94143-0610, USA.
J Cardiovasc Risk (England) Jun 1994, 1 (1) p75-80
BACKGROUND: Dietary consumption of fish, rich in n-3 polyunsaturated
fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA),
has been shown to reduce blood pressure in both animal studies and
clinical trials. Although the antihypertensive mechanisms are not known,
the blood-pressure-lowering effect of n-3 polyunsaturated fatty acids
may be partially attributed to their vasorelaxant properties.
METHODS: Aortic rings with and without endothelium, from Wistar-Kyoto
(WKY) and spontaneously hypertensive rats (SHR), 16-17 weeks old, were
suspended in tissue baths and isometric tension was measured.
Concentration-response curves were generated for DHA and EPA (1-100 mu
mol/l) in norepinephrine-contracted rings. Blood pressure was measured
using the tail-cuff method and aortic media thickness was determined.
RESULTS: Blood pressure was significantly increased in SHR (n=10; 194
+/- 4.4 mmHg) compared with WKY (n=10; 124 +/- 1.2 mmHg, P < or =
0.0001). DHA (1-100 mu mol/l) relaxed aortic rings f rom WKY (-3.3 +/-
0.7 to -13 +/- 2.3%, P < or = 0.001) and from SHR (-6.5 +/- 1.8 to
-22.9 +/- 4%, P < or = 0.01) in a concentration-dependent manner. EPA
(1-100 mu mol/l) evoked greater relaxation in SHR (-10.1 +/- 2.0 to -33
+/- 3.9%, P < 0.01) than in WKY (-2.9 +/- 1.1 to -18.3 +/- 2.1%, P
< 0.01) aortic rings. The relaxant effect of DHA in both WKY and SHR
and of EPA in WKY were not dependent on an intact endothelium. However,
EPA (1-10 mu mol/l) induced greater responses in intact SHR rings (-10.1
+/- 2.0 to -14.5 +/- 3.1%) than in de-endothelialized SHR rings (0 to
-2.1 +/- 1.7%, P = 0.001).
CONCLUSION: The direct relaxant effects of n-3 fatty acids as seen in
WKY and SHR may contribute, in part, toward the blood-pressure-lowering
effect of dietary fish and fish-oil supplementation.
^TOP^
Effects of a combination
of evening primrose oil (gamma linolenic acid) and fish oil
(eicosapentaenoic + docahexaenoic acid) versus magnesium, and versus
placebo in preventing pre-eclampsia.
D'Almeida A; Carter JP; Anatol A; Prost C
Nutrition Program, School of Public Health and Tropical Medicine, Tulane
University, New Orleans, LA.
Women Health (United States) 1992, 19 (2-3) p117-31
In a placebo controlled, partially double-blinded, clinical trial, a
combination of evening primrose oil and fish oil was compared to
Magnesium Oxide, and to a Placebo in preventing Pre-Eclampsia of
Pregnancy. All were given as nutritional supplements for six months to a
group of primiparous and multiparous pregnant women. Some of these women
had personal or family histories of hypertension (21%). Only those
patients who received prenatal care at the Central Maternity Hospital
for Luanda were included in the study. Compared to the Placebo group
(29%), the group receiving the mixture of evening primrose oil and fish
oil containing Gamma-linolenic acid (GLA), Eicosapentaenoic acid (EPA),
and Docosahexaenoic acid (DHA) had a significantly lower incidence of
edema (13%, p = 0.004). The group receiving Magnesium Oxide had
statistically significant fewer subjects who developed hypertension of
pregnancy. There were 3 cases of eclampsia, all in the Placebo group.
^TOP^
Antithrombotic activity
of garlic: its inhibition of the synthesis of thromboxane-B2 during
infusion of arachidonic acid and collagen in rabbits.
Ali M; Thomson M; Alnaqeeb MA; al-Hassan JM; Khater SH; Gomes SA
Department of Biochemistry, Faculty of Science, Kuwait University.
Prostaglandins Leukot Essent Fatty Acids (Scotland) Oct 1990, 41 (2)
p95-9
Rabbits were given collagen and arachidonic acid intravenously. Blood
pressure, platelet counts, plasma thromboxane-B2 (TXB2) and plasma
6-keto-prostaglandin F1 alpha, (6-keto-PGF1 alpha) were determined. Both
thrombogenic agents, upon infusion of a lethal dose, caused
thrombocytopenia, indicative of in vivo platelet aggregation and
hypotension. These changes were associated with an increase in plasma
levels of TXB2 and 6-keto-PGF1 alpha measured by radioimmunoassay (RIA).
Pretreatment of rabbits with an aqueous extract of garlic (500 mgkg)
provided protection from thrombocytopenia and hypotension.
Thromboxane-B2 synthesis was significantly reduced in animals pretreated
with garlic and then injected with a lethal dose of either collagen or
arachidonic acid. The amount of TXB2 synthesized in these animals was
not sufficient to induce thrombocytopenia or hypotension. All animals
pretreated with garlic were well protected against the effects of
collagen or arachidonate infusion, and no apparent symptoms were
observed in these animals. These observations indicate that garlic may
be beneficial in the prevention of thrombosis.
^TOP^
Bulgarian traditional
medicine: a source of ideas for phytopharmacological investigations.
Petkov V
J Ethnopharmacol (Switzerland) Feb 1986, 15 (2) p121-32
Some data about the use of medicinal plants in Bulgarian traditional
medicine in the Middle Ages and in modern times are presented and the
results of 40-year-long experimental-pharmacological investigations on
many medicinal plants used in Bulgarian traditional medicine are
reviewed. In-depth discussion is presented on the investigations of
garlic (Allium sativum L.), a plant widely used by Bulgarian people for
treating different diseases. Data from studies on a large number of
plants used for treatment of hypertension, infectious diseases and as
diuretic and spasmolytic remedies are summarized.
^TOP^
Garlic as a natural agent
for the treatment of hypertension: a preliminary report.
Foushee DB; Ruffin J; Banerjee U
Cytobios (England) 1982, 34 (135-36) p145-52
The major objective of this study was to re-evaluate the effects of
garlic on blood pressure with respect to its ability to provoke a
decrease in blood pressure and to determine the length of time that this
decrease would require. Spontaneously hypertensive rats were given three
doses of garlic extract (0.1 ml/kg, 0.25 ml/kg, and 0.5 ml/kg) by oral
injection. The blood pressures of these ether-anaesthetized rats were
measured immediately before the extract was given, and then 0.5, 2, 4,
6, and 24 h after the extract was given. A blood pressure measurement
was also taken at 48 h after extract administration for the 0.5 ml/kg
dose. The Gilson Duograph System was used to measure blood pressure by
the tail-cuff method. There was a marked decrease in the systolic blood
pressure of all of the rats after three doses and the decrease occurred
within 30 min in each case. Even though the average decreases for the
0.1 ml/kg and the 0.25 ml/kg doses were calculated as 51,25 mm Hg and
56.25 mm Hg, respectively, these doses were not sufficient to sustain
the blood pressure in a normal range for more than 1 or 2 h. The 0.5
ml/kg dose, showing an average decrease of 65.7 mm Hg, was sufficient to
provoke a decrease to a normal level and to sustain this decrease for up
to 24 h. The results indicate that garlic is effective as a natural
agent for the treatment of hypertension.
^TOP^
The decline in stroke
mortality. An epidemiologic perspective.
Klag MJ; Whelton PK
Department of Medicine, Johns Hopkins University School of Medicine,
Baltimore, MD.
Ann Epidemiol (United States) Sep 1993, 3 (5) p571-5
The evidence that treatment of hypertension prevents stroke is
incontrovertible. Several observations, however, suggest that
improvements in the prevalence of antihypertensive treatment cannot
explain all of the recent decline in stroke mortality. Changes in
nutritional patterns may explain some of the observed decline.
Prospective studies have demonstrated conclusively an independent,
increasing risk of hemorrhagic, but not thrombotic, stroke at higher
levels of alcohol use. Stroke mortality is associated inversely with fat
and protein intake. Dietary sodium has been linked to stroke in ecologic
studies but not in prospective studies. Ecologic studies have suggested
that foods high in Vitamin-C and potassium protect against stroke; an
inverse association of potassium intake with fatal stroke has been
demonstrated in cohort studies. Two studies in humans also suggest a
protective effect of serum selenium against subsequent stroke.
Determination of the influence of nutrients on stroke incidence offers
tantalizing opportunities for future research and possibly,
intervention.
^TOP^
Antioxidant therapy in
the aging process.
Deucher GP
Clinica Guilherme Paulo Deucher, Sao Paulo, Brazil.
EXS (Switzerland) 1992, 62 p428-37
A total of 1,265 patients with age-related diseases such as diabetes,
arthritis, vascular disease and hypertension as well as 1,100 persons in
diminished health without apparent disease, were treated with the metal
chelator EDTA and antioxidants such as vitamin C, E, beta-carotene,
selenium, zinc and chromium. Good results were observed in the majority
of patients. This is encouraging for the initiation of controlled
clinical trials.
^TOP^
Antioxidants show an
anti-hypertensive effect in diabetic and hypertensive subjects.
Ceriello A; Giugliano D; Quatraro A; Lefebvre PJ
Cattedra di Diabetologia e Dietoterapia I Facolta di Medicina,
Universita di Napoli, Italia.
Clin Sci (Colch) (England) Dec 1991, 81 (6) p739-42
1. In this study an acute anti-hypertensive effect of three
anti-oxidant agents (Vitamin-C, thiopronine and glutathione) in
hypertensive subjects and in both hypertensive and non-hypertensive
diabetic patients is reported.
2. The antioxidants had no effect on blood pressure in healthy normal
subjects at a dose of 6 mmol, but thiopronine and glutathione produced a
significant hypotensive effect at a dose of 12 mmol.
3. These data suggest that antioxidants might have a dilatatory
effect and that an imbalance of the nitric oxide-free radical
interaction might facilitate the development of hypertension in humans.
^TOP^
[Relation between
Vitamin-C consumption and risk of ischemic heart disease]
Davydenko NV, Kolchinskii VI
Vopr Pitan 1983 Nov-Dec;(6):17-9
Interrelation was studied between Vitamin-C consumption and the
prevalence of coronary heart disease and some risk factors in a
non-organized male population in Kiev. A reverse relationship was
established between Vitamin-C consumption, the prevalence of coronary
heart disease and some risk factors, such as arterial hypertension,
hyperlipoproteinemia and overweight.
^TOP^
Blood pressure and
nutrient intake in the United States.
McCarron DA; Morris CD; Henry HJ; Stanton JL
Science (United States) Jun 29 1984, 224 (4656) p1392-8
A data base of the National Center for Health Statistics, Health and
Nutrition Examination Survey I (HANES I), was used to perform a
computer-assisted, comprehensive analysis of the relation of 17
nutrients to the blood pressure profile of adult Americans. Subjects
were 10,372 individuals, 18 to 74 years of age, who denied a history of
hypertension and intentional modification of their diet. Significant
decreases in the consumption of calcium, potassium, vitamin A, and
Vitamin-C were identified as the nutritional factors that distinguished
hypertensive from normotensive subjects. Lower calcium intake was the
most consistent factor in hypertensive individuals. Across the
population, higher intakes of calcium, potassium, and sodium were
associated with lower mean systolic blood pressure and lower absolute
risk of hypertension. Increments of dietary calcium were also negatively
correlated with body mass. Even though these correlations cannot be
accepted as proof of causation, they have implications for future
studies of the association of nutritional factors and dietary patterns
with hypertension in America.