Impairment of central mediation of the arterial baroreflex by acute ethanol administration.

We investigated the possibility that the impairment of baroreflex control of heart rate was due to an action of ethanol on the central component of the baroreflex arc. Baroreceptors and baroreceptor afferents were removed from the arc by sino-aortic denervation and the central end of the left aortic depressor nerve was stimulated. Stimulation frequency response curves relating the decreases in blood pressure, heart rate and sympathetic efferent nerve discharge to the frequency of stimulation were constructed before and after the administration of 0.33, 0.66 and 1 g/kg of ethanol administered systemically. Except for a small decrease in blood pressure following the 1 g/kg dose, ethanol administration did not produce any change in baseline heart rate or blood pressure but the frequency response curve of heart rate was reset by the two lower doses of ethanol whereas the dose of 1 g/kg produced frank impairment of baroreflex control. Similarly the dose of 1 g/kg also impaired the depressor response to aortic nerve stimulation whereas it did not impair the baroreflex control of sympathetic efferent discharge. These data suggest a differential effect of ethanol on central pathways that control baroreflex responses. To ensure that the effect of ethanol was not due to an action of ethanol on an end organ, the heart, a separate group of rats were prepared with sino-aortic denervation and the peripheral end of the cut right vagus nerve was stimulated with increasing frequency. Ethanol did not affect the response to stimulation of the vagus nerve showing that the impairment of baroreflex control of cardiovascular variables was primarily of central origin.