Role of aortic baroreceptors in ethanol-induced impairment of baroreflex control of heart rate in conscious rats

This study investigated the relative contribution of aortic baroreceptors to the depressant effect of ethanol on arterial baroreceptor function. The acute hemodynamic effects of ethanol were studied in conscious freely moving aortic baroreceptor denervated (ABD) and sham-operated (SO) rats. ABD but not the sham operation caused immediate and significant (P < .05) increases in mean arterial pressure and heart rate (HR) and an impairment of the baroreflex-mediated control of HR (baroreflex sensitivity, BRS). Two to three days after ABD, these parameters, except the BRS, subsided to near-control levels. Both operations (ABD and sham) significantly reduced the daily water intake but the reduction was significantly greater in ABD rats. Intravenous administration of ethanol (0.1, 0.5 or 1.0 g/kg) to either SO or ABD rats produced short-lived dose-related pressor and brady-cardiac responses which correlated well with blood ethanol concentration. In SO rats, ethanol caused dose-related decreases in the slopes of the curves relating increments in mean arterial pressure induced by phenylephrine to corresponding bradycardic responses; the higher dose significantly (P < .05) reduced the slope from - 2.03 ± 0.14 to -1.28 ± 0.18 beats/min/mm Hg, indicating an impairment of BRS. Conversely, in ABD rats, ethanol failed to influence the BRS; the slopes before and after ethanol (1 g/kg) were similar (-1.1 ± 0.07 vs. -1.0 ± 0.23 beats/min/mm Hg). The lack of ethanol effect in ABD rats cannot be accounted for by the assumption that aortic barodenervation depressed the baroreceptor reflex to its nadir or by a difference in concentration of blood ethanol. Pentobarbital caused further attenuation of the HR response to phenylephrine in ABD rats (slopes were -0.46 ± 0.03 vs. -1.2 ± 0.06 beats/min/mm Hg) and blood ethanol concentrations were very similar in ABD and SO rats. The data suggest that ethanol impairs the HR response to stimulation of arterial baroreceptors through a mechanism that mainly involves aortic baroreceptors and that the acute hemodynamic effects of ethanol are not dependent on aortic baroreceptors.