Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats

Abdel-Rahman, A-R.A.; Russ, R. D.; Strickland, Judy; Wooles, W. R.

doi:10.1139/y87-134

Cited by 61 publications

(49 citation statements)

References 12 publications

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“…However, recent findings from our laboratory strongly suggest directionally opposite hemodynamic and electrophysiological effects for ethanol as compared with the well-documented effects of clonidine. Even in doses that had no significant effect on baseline blood pressure, our own data 16 - 17 and those of others 18 -20 have shown that ethanol increased baseline heart rate. Child et al 31 suggested the positive chronotropic effect of ethanol is mediated by sympathetic overactivity that was sufficient to mask its cardiodepressant effect.…”

Section: Discussionsupporting

confidence: 37%

“…The method described in our previous study 16 was used for instrumentation of the rats for measurement of blood pressure and heart rate and for intravenous administration of drugs. The rats were anesthetized by methohexital (Brevital, Eli Lilly and Co., Indianapolis, Indiana; 50 mg/kg i.p).…”

Section: Methodsmentioning

confidence: 99%

“…For example, clonidine and guanabenz lower blood pressure and heart rate mainly via a central mechanism of action that involves a decrease in central sympathetic tone. 12 -14 On the other hand, even though alcohol does not change blood pressure after its acute administration, 15 -17 it increases heart rate, 16 -18 sympathetic efferent discharge, 19 and circulating levels of catecholamines. 20 Also, both alcohol and clonidine influence differently the baroreceptor reflexes.…”

Section: Reversal By Ethanol Of the Hypotensive Effect Of Clonidine Imentioning

confidence: 99%

“…The doses of phenylephrine employed in this study were shown to have negligible direct chronotropic effects in our previous study. 16 The peak increases in mean arterial pressure and the associated reflex bradycardia were used to calculate the baroreceptor reflex slope with a linear regression analysis for individual rats. Baroreceptor reflex curves were constructed by plotting the evoked increases in mean arterial pressure, in increments of 10 mm Hg, against the concomitant decreases in heart rate.…”

Section: Measurement Of Baroreceptor Reflex Sensitivitymentioning

confidence: 99%

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Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Abdel‐Rahman

1989

Hypertension

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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<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;14:531-541)

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Section: Discussionsupporting

confidence: 37%

Section: Methodsmentioning

confidence: 99%

Section: Reversal By Ethanol Of the Hypotensive Effect Of Clonidine Imentioning

confidence: 99%

Section: Measurement Of Baroreceptor Reflex Sensitivitymentioning

confidence: 99%

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Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Abdel‐Rahman

1989

Hypertension

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“…43 Narkiewicz et al 44 reported that alcohol enhances the hypotension induced by lower body negative pressure. The combination of impairment of the baroreceptor reflex and systemic vasodilation acts to potentiate orthostatic hypotension and may induce syncope after drinking in susceptible subjects.…”

Section: Neurohormonal Actions Of Alcoholmentioning

confidence: 99%

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Kawano

2010

Hypertens Res

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Alcohol has complex effects on the cardiovascular system. The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role in hypertension and cardiovascular disease. The relationship between alcohol and hypertension is well known, and a reduction in the alcohol intake is widely recommended in the management of hypertension. Moreover, alcohol has both pressor and depressor actions. The latter actions are clear in Oriental subjects, especially in those who show alcohol flush because of the genetic variation in aldehyde dehydrogenase activity. Repeated alcohol intake in the evening causes an elevation in daytime and a reduction in nighttime blood pressure (BP), with little change in the average 24-h BP in Japanese men. Thus, the hypertensive effect of alcohol seems to be overestimated by the measurement of casual BP during the day. Heavy alcohol intake seems to increase the risk of several cardiovascular diseases, such as hemorrhagic stroke, arrhythmia and heart failure. On the other hand, alcohol may act to prevent atherosclerosis and to decrease the risk of ischemic heart disease, mainly by increasing HDL cholesterol and inhibiting thrombus formation. A J-or U-shaped relationship has been observed between the level of alcohol intake and risk of cardiovascular mortality and total mortality. It is reasonable to reduce the alcohol intake to less than 30 ml per day for men and 15 ml per day for women in the management of hypertension. As a small amount of alcohol seems to be beneficial, abstinence from alcohol is not recommended to prevent cardiovascular disease. INTRODUCTIONAlcohol has complex effects on the cardiovascular system. The relationship between alcohol and hypertension is well known, and a restriction of alcohol intake is widely recommended as a part of lifestyle modifications in the management of hypertension. 1-6 Alcohol has both pressor and depressor actions, however, and the genetic susceptibility regarding alcohol metabolism influences the cardiovascular effect of alcohol. 3,7 The effect of alcohol on blood pressure (BP) is also modified by several factors, such as the level of consumption, time period after the last drink and overall drinking behavior.Alcohol consumption is associated with several cardiovascular diseases, such as brain hemorrhage, heart failure and arrhythmia, as well as with other disorders. 3,[8][9][10][11] Heavy drinking and alcoholism not only lead to medical problems but are also serious social concerns. However, alcohol also seems to have beneficial effects, including the prevention of ischemic heart disease. It has been shown that cardiovascular and all-cause mortality is lower in light drinkers compared with nondrinkers. 3,[8][9][10][11][12] The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role

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Central Neural Mechanisms in the Cardiovascular Effects of Ethanol

Kunos¹,

Varga²,

Zakhari³

1992

Central Neural Mechanisms in Cardiovascular Regulation

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Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats

Cited by 61 publications

References 12 publications

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Central Neural Mechanisms in the Cardiovascular Effects of Ethanol

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