Direct evidence for selective involvement of aortic baroreceptors in ethanol-induced impairment of baroreflex control of heart rate.

In a previous study, we have shown that ethanol reduced baroreflex control of heart rate (baroreflex sensitivity, BRS) in conscious sham-operated (SO) rats, but not in aortic barodenervated rats, which suggested, by elimination, a role for aortic baroreceptors in the depressant effect of ethanol on BRS. The present study sought direct evidence to support the hypothesis that aortic baroreceptors are selectively influenced by ethanol. The effect of ethanol on BRS measured by evoked increments (phenylephrine) and decrements (nitroprusside) in blood pressure was studied in conscious unrestrained carotid barodenervated (CBD) and SO rats. The experiments were carried out on 2 consecutive days in the same rats and used phenylephrine on one day and nitroprusside on the other. Compared to sham operation, CBD caused an acute rise in mean arterial pressure and heart rate and a significant reduction in BRS. Two days later, mean arterial pressure and heart rate of conscious unrestrained CBD rats subsided to control levels, whereas baroreflex-mediated bradycardic and tachycardic responses were 65 and 35%, respectively, of control values. Administration of ethanol (1 g/kg) produced similar brief pressor and bradycardic responses in CBD and SO rats. In spite of a significantly lower BRS in CBD as compared to SO rats, ethanol (1 g/kg) caused a significant (P < .05) and comparable attenuation of BRS measured by the response to phenylephrine in CBD and SO rats (30% vs. 38%). In contrast, ethanol caused slight nonsignificant reductions in BRS measured by the response to nitroprusside in CBD and SO rats. Blood ethanol concentrations were similar in both groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS)