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  • Title: Effect of acute ethanol administration on the baroreceptor reflex control of heart rate in normotensive human volunteers.
    Author: Abdel-Rahman AR, Merrill RH, Wooles WR.
    Journal: Clin Sci (Lond); 1987 Jan; 72(1):113-22. PubMed ID: 3802717.
    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.
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