Effect of acute ethanol administration on the baroreceptor reflex control of heart rate in normotensive human volunteers

Abstract

The effects of acute ethanol administration on blood pressure, heart rate and the baroreceptor reflex control of heart rate were studied in normotensive subjects who served as their own control. Baroreceptor reflex control of heart rate was measured by two methods: the ramp method and the steady state method. None of the doses of ethanol had any effect on blood pressure during the observation period, except for the highest dose where a slight elevation was evident for a short period of time. On the other hand, the heart rate showed a slight but consistent dose-related increase. In general, ethanol attenuated the baroreceptor mediated bradycardia but this effect was dependent on the way in which blood pressure was elevated. A dose-related impairment of baroreceptors was evident when the ramp method was used, i.e. ethanol significantly depressed baroreflex sensitivity, expressed as delta heart period (HP)/delta mean arterial pressure (MAP). In contrast, delta HP/delta MAP was not influenced by ethanol when the steady state method was used. However, the steady state baroreflex curves were reset about a higher median blood pressure (MAP50), suggesting that the baroreceptors will be operative at higher blood pressure levels after ethanol. The pressor responsiveness was also influenced differently by ethanol depending on the method of injecting phenylephrine. An increase in pressor responsiveness was evident, though not dose-related, after ethanol only when blood pressure was elevated by the ramp method, suggesting that the inverse relationship between baroreflex sensitivity and pressor responsiveness is more prominent with the ramp method and/or when impairment rather than resetting of baroreceptors occurs. That the decrease in baroreflex sensitivity and the increase in MAP50 were related to peak ethanol levels in blood and that the blood pressure was not influenced by ethanol strongly suggest these effects were ethanol mediated. The weakened buffering action of the baroreflexes would be expected to favour the development of higher blood pressure.

Alcohol and arrhythmias: a comprehensive review

“…Animal and normal human volunteer studies have confirmed similar acute, as well as chronic, effects of alcohol on baroreceptor responsiveness (40,41).. Gender-related differences in baroreceptor reflex control mechanisms have been demonstrated which might explain different dose response relationships between alcohol and arrhythmias in males and females (42).…”

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

“…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.…”

“…17 It is possible that larger doses of ethanol would attenuate further the hypotensive effect of clonidine. We decided, however, to use a dose of ethanol that resulted in a blood ethanol concentration of 54.2±6.3 mg/dl, which is comparable to that attained after social drinking.…”

“…21 -23 In the present study and in agreement with reported findings, 21 -23 we observed that clonidine-evoked lowering of arterial pressure was associated with a substantial increase in baroreceptor reflex slopes. Based on our previous findings, which showed ethanol produced 17 we decided to investigate the possibility of whether this effect, which is directionally opposite to that of clonidine, 21 -23 is involved in ethanol-clonidine interaction. The data of the present investigation clearly demonstrated that ethanol virtually abolished the augmentatory action of clonidine on baroreceptor reflexes ( Figure 4) along with attenuating its hypotensive effect (Figures 2 and 3).…”

Cardiovascular and cutaneous responses to the combination of alcohol and soft drinks: the way to orthostatic intolerance?

“…Interestingly, alcohol may decrease myocardial contractility in healthy young people (Kelly et al, 1996), already evident at concentrations corresponding to the legal driving limit of 0.5 0 / 00 common in most Western Europe. In addition, alcohol depresses the vasoconstrictor response to noradrenaline infusion (Eisenhofer et al, 1984) and may interfere with the autonomic nervous system, as it disrupts the vasoconstrictor response to orthostatic stress (Narkiewicz et al, 2000;Carter et al, 2011), and impairs baroreflex function (Abdel-Rahman et al, 1987;Carretta et al, 1988). In this context, it comes to no surprise that alcohol consumption may induce orthostatic hypotension, even in young, healthy subjects.…”