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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of ethanol (alcohol) consumption on blood pressure during and after the development of hypertension was examined by using spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP). Normotensive Wistar-Kyoto (WKY) rats were also used for comparison. Substituting alcohol (5-20%) for drinking water at 1 month of age retarded the age-dependent rise of blood pressure in all three strains so that, at 7 months, blood pressure measured by a tail-cuff method was 24 mm Hg, 26 mm Hg, and 41 mm Hg lower in the alcohol-treated WKY rats, SHR, and SHRSP, respectively, than in untreated rats. Significant differences in blood pressure were seen in each strain after only 3 months. Withdrawal of alcohol at this stage caused an acute rise of blood pressure then a return to subnormal levels, which persisted for a further 3 months. Administration of 15% alcohol to adult WKY rats and SHR for 2 months had no significant effect on blood pressure. Increasing alcohol content to 20% for a further 2 months prevented rises of blood pressure in both strains. Thus, although continuous drinking of alcohol does not lower blood pressure, it appears to counteract the development of hypertension in rats.
Hypertension 1989 Jun
PMID:Antihypertensive effect of alcohol in spontaneously hypertensive rats. 273 9

Cardiovascular effects of NC-1100 (1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl)ethanol and possible modes of action were studied in dogs and guinea pigs. 1. In pentobarbital-anesthetized dogs, intravenous administration of NC-1100 (0.05-1.6 mg/kg) induced a dose-dependent fall of blood pressure, a bradycardia followed by temporal tachycardia, a slight and transient stimulation of respiration and a prolongation of the R-R interval with slight augmentations of P, R and T waves in ECG. 2. In pentobarbital-anesthetized dogs, NC-1100 (2.5-80 micrograms/kg) administered to the maxillary and vertebral artery dose-dependently increased the blood flow in the respective artery. 3. Intravenous administration of NC-1100 (0.05-1.6 mg/kg) also exhibited dose-dependent increases of the maxillary and vertebral blood flow, though the increase in maxillary flow was a little reduced at a high dose of 1.6 mg/kg. Intravenous administration of NC-1100 (0.1-1.6 mg/kg) caused a slight increase in the aortic and coronary blood flow, a decrease in renal flow and a slight and transient decrease followed by an increase in femoral flow. 4. In pentobarbital-anesthetized dogs, NC-1100 (1 mg/kg) administered i.v. did not affect responses of blood pressure and heart rate to norepinephrine and isoprenaline (isoproterenol) but slightly inhibited hypotensive responses to acetylcholine. NC-1100 had no effect on hypertension elicited by carotid sinus reflex and on bradycardia by vagus stimulation. NC-1100 slightly inhibited the tachycardia elicited by pre- as well as postganglionic stellate stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular effects of 1-(3,4-dimethoxyphenyl)-2-(4-diphenylmethylpiperazinyl) ethanol and possible mechanisms involved. 275 31

In 15 patients with renovascular hypertension, considered unsuitable for angioplasty or surgery, percutaneous renal ablation was performed by injection of ethanol into the renal vasculature. Partial or complete renal ablation was confirmed by follow-up intravenous pyelography or arteriography. Patients were followed-up for a mean of 24.8 months after therapy and blood pressure was improved in all patients with five being cured. This study shows that percutaneous renal ablation is a useful and successful method of therapy for renal hypertension, and that it should be considered in patients unsuitable for surgery or angioplasty.
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PMID:Total or partial percutaneous renal ablation in the treatment of renovascular hypertension: radiological and clinical aspects. 275 46

To determine whether or not the previously reported association between alcohol intake and high blood pressure is influenced by differential intake of calcium and potassium in drinkers compared with nondrinkers and to assess the magnitude of the independent contributions of alcohol, calcium, and potassium to blood pressure, these associations were evaluated in 7,011 men of Japanese descent. Categorical analyses and multiple linear regression techniques were used to test the hypotheses that alcohol, calcium, and potassium were independent predictors of blood pressure. Alcohol consumption above a threshold of approximately 20 ml/day was found to be positively, strongly, and independently correlated with systolic and diastolic pressures, and this effect was completely independent of the effects of calcium and potassium. Calcium and potassium intake were highly correlated (r = 0.59) and were inversely related to blood pressure, and their combined effect was greater than the effect of either alone. However, in the subgroup of moderate and heavier drinkers, only potassium was inversely related to blood pressure. This finding is compatible with previous reports of malabsorption and increased excretion of calcium at higher levels of alcohol intake, and it indicates that a small portion of the alcohol-induced blood pressure elevation may be mediated through calcium depletion. In the range of dietary intake in this cohort, the effect of alcohol on blood pressure was stronger than was either the separate or combined effects of calcium and potassium.
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PMID:Dietary alcohol, calcium, and potassium. Independent and combined effects on blood pressure. 276 13

We investigated the acute hemodynamic effects of ethanol microinjection into brain areas known to influence cardiovascular function and reflexes. In chloralose-anesthetized rats, ethanol had no effect on baseline mean arterial pressure, heart rate, or sympathetic efferent discharge when microinjected into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, the rostral ventrolateral medulla, or the posterior hypothalamus. On the other hand, ethanol microinjection into the anterior hypothalamus caused a site-dependent pressor effect and an increase in sympathetic efferent discharge. Baroreceptor heart rate response but not sympathetic efferent discharge response was impaired by ethanol microinjection into the nucleus tractus solitarius, the dorsal motor nucleus of the vagus, and the rostral ventrolateral medulla, suggesting that ethanol involves one or more of these areas in its inhibitory effect on baroreceptor heart rate response and that ethanol has a selective action on baroreceptor reflex control of heart rate. The findings that 1) the effect was dose dependent and 2) injection of ethanol outside of, or an equal volume of cerebrospinal fluid into, the nucleus tractus solitarius had no effect on the response strongly suggest that the observed effect on baroreceptor heart rate response was ethanol mediated. Ethanol microinjection into the dorsal motor nucleus of the vagus impaired the heart rate response, thus raising the possibility that leakage of ethanol to that area from the nucleus tractus solitarius might have contributed to its effect. These findings show that ethanol has a pressor and sympathoexcitatory site of action within the anterior hypothalamus and that it selectively impairs baroreceptor heart rate response via a central site of action; the mechanisms by which ethanol produces these effects remain to be elucidated.
Hypertension 1989 Sep
PMID:Impairment of baroreceptor reflex control of heart rate but not sympathetic efferent discharge by central neuroadministration of ethanol. 276 59

The development of blood pressure was monitored by the tail-cuff method in normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) receiving ethanol (alcohol) in drinking water from weaning (approximately 1 month of age). Alcohol administration over a 3-month period attenuated the development of hypertension in SHRSP and also caused a small reduction of the initial blood pressure rise in WKY. This was accompanied by a reduction of fluid intake and an increase of circulating antidiuretic hormone (arginine vasopressin; AVP). Circulatory volume remained constant. Direct measurement of arterial blood pressure in conscious rats before and after autonomic blockade confirmed the antihypertensive effect of alcohol in SHRSP and indicated that it is at least partly dependent on altered activity of neural mechanisms. Sudden withdrawal of alcohol caused an immediate increase of fluid intake followed by a rise of blood pressure lasting several days in both WKY and SHRSP. This withdrawal hypertension could not be attributed to changes in plasma catecholamines or AVP.
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PMID:Effects of chronic alcohol consumption and alcohol withdrawal on blood pressure in stroke-prone spontaneously hypertensive rats. 276 25

The effects of prolonged infusions of ethanol on endothelium-dependent vasorelaxation induced by acetylcholine and adenosine triphosphate (ATP) and on endothelium-independent relaxation induced by papaverine were studied and compared in isolated perfused rat mesenteric artery preparations. Infusion of ethanol over 60 minutes at concentrations of 1.6, 4.7, 6.3, and 7.9 mg/ml caused concentration-related inhibition of norepinephrine-induced vasoconstriction. In preparations infused with 6.3 and 7.9 mg/ml, this effect reached a maximum after 10-20 minutes but had vanished by the end of the infusion; 1 hour after the end of the infusion, the effects of norepinephrine were potentiated by 71% and 108%, respectively. Acetylcholine-induced vasorelaxation (EC50 3.0 ng/ml in controls) was significantly reduced after 6.3 mg/ml ethanol infusion and totally abolished after 7.9 mg/ml ethanol infusion. ATP-induced vasorelaxation (EC50 180 ng/ml in controls) was also abolished after 7.9 mg/ml of ethanol infusion. By contrast, the vasorelaxant effects of papaverine were not affected by 7.9 mg/ml ethanol infusion. Light-microscopic examination revealed that the endothelial cells were present in ethanol-treated and in control mesenteric arterial beds. These observations indicate that ethanol suppresses endothelium-dependent vasorelaxation without apparent removal of the endothelial cells. The compromised relaxant capacity of the endothelium after ethanol and the resultant intensification of the vasoconstrictor response to norepinephrine may contribute to the development of vascular diseases such as hypertension and stroke.
Hypertension 1989 Jun
PMID:Alcohol suppresses endothelium-dependent relaxation in rat mesenteric vascular beds. 278 50

We studied the acute effect of ethanol on the hypotensive response to clonidine in conscious spontaneously hypertensive rats. When administered during the hypotensive response to clonidine, ethanol not only reversed the response but also caused a slight but significant short-lived pressor effect. The maximal hypotensive effect of graded doses of clonidine was significantly (p less than 0.05) attenuated by a dose of 1 g/kg ethanol, which resulted in a peak blood ethanol concentration of 54.2 +/- 6.3 mg/dl. The data strongly suggest the adverse effect of ethanol on the hypotensive response to clonidine is ethanol mediated and that their antagonistic interaction is both reversible and reproducible because: 1) an equal volume of saline had no effect on the hemodynamic responses to clonidine and 2) crossing over ethanol and saline treatments on days 2 and 3, which allowed longitudinal comparisons, showed that the effect of ethanol was similar both in naive rats (day 1) and in rats that were pre-exposed to ethanol (day 3). Whether this negative effect of ethanol also involves other antihypertensive agents that do not act primarily by a central nervous system mechanism was investigated. The same dose of ethanol had little or no effect on the hypotensive response to hydralazine, suggesting the negative effect of ethanol is selective to centrally acting antihypertensive agents. Although the mechanism by which ethanol reverses the hypotensive effect of clonidine is not known, it is possible that it involves an ethanol-evoked increase in plasma catecholamine levels, which are known to be decreased by clonidine. That ethanol did not reverse the hypotensive effect of hydralazine, which is also known to be associated with increased plasma catecholamine levels, supports this notion. The findings of the present study may explain, at least in part, why regular use of alcohol is associated with an inadequate control of blood pressure in treated hypertensive patients who are regular consumers of alcohol.
Hypertension 1989 Nov
PMID:Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats. 280 15

The development of a novel model of human alcoholism has involved the presentation of a 30% alcohol solution to Sprague-Dawley rats via a syringe-feeding needle apparatus. With twice daily intermittent drinking, rats consumed an equivalent of 7-8 g/kg body weight of alcohol, which represented 25% of total daily caloric intake. Alcohol was absorbed rapidly, as significant circulating concentrations were observed within 15 min of gavage, eventually peaking at approximately 200 mg% 1 h later. Hemodynamic recordings in the conscious state after a 10-week drinking program indicated a normotensive blood pressure at peak blood alcohol levels, yet a hypertensive response 24 h after the final drink at a time when blood alcohol was not detected. Alcoholic rats continued to gain weight in parallel with controls fed ad libitum throughout the study, and changes in cardiac size and indices of contractility were not affected by 10 weeks of intermittent drinking. Additionally, no histological evidence of cardiac muscle damage was observed in alcoholic animals. Our animal model closely resembles the clinical situation in terms of the pattern of alcohol consumption, circulating concentrations of alcohol and the percentage of caloric intake in the form of alcohol. The hemodynamic changes observed support the hypothesis that alcoholic hypertension may be a manifestation of withdrawal, as opposed to any direct pressor effect of alcohol itself.
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PMID:Cardiovascular effects of intermittent drinking: assessment of a novel animal model of human alcoholism. 280 92

The prevalence of heavy alcohol consumption is a major problem of increasing proportions throughout the world. Although alcohol sensitizing drugs and more recently serotonin uptake inhibitors are drug interventions with some following, their long term beneficial consequences have yet to be demonstrated. In recent years, we have demonstrated that manipulating activity in the renin-angiotensin system will dramatically alter voluntary alcohol consumption in rats. Based on these findings, the present study evaluated the ability of a class of drugs known as the angiotensin converting enzyme inhibitors to reduce voluntary alcohol drinking in laboratory animals. These drugs prevent the conversion of angiotensin I to angiotensin II. They have been licensed for use in Europe and North America and are indicated in the treatment of hypertension. Our experiments showed that both captopril (Capoten, Squibb) and enalapril (Vasotec, Merck Sharpe & Dohme) can reduce alcohol drinking in both normotensive and hypertensive animals regardless of whether the pattern of intake is in a bout or of a less exaggerated nature. Furthermore, this change in alcohol intake can occur without concomitant changes in blood pressure, plasma renin activity, overall fluid balance, or the distribution and metabolism of alcohol. Taken together these findings suggest that the angiotensin converting enzyme inhibitors should be evaluated in a clinical setting for they may prove to be a useful new treatment or treatment adjunct for alcohol abuse in humans.
Alcohol Clin Exp Res 1988 Feb
PMID:Angiotensin converting enzyme inhibitors: animal experiments suggest a new pharmacological treatment for alcohol abuse in humans. 283 50


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