ABSTRACT
There is considerable epidemiological evidence that suggests a positive relationship between ethanol consumption and arterial blood pressure [1-5]. However, the mechanism by which ethanol elevates blood pressure is not known. We have performed a number of studies to test the hypothesis that ethanol-associated hypertension may be a consequence of ethanol-evoked attenuation of baroreflex activity. Our earlier findings in animals [6-8] were the first to describe the effect of ethanol on the baroreflex mediated bradycardic response. An earlier clinical study showed that moderate amounts of ethanol enhanced the reflex tachycardic response triggered by the Valsalva maneuver and body tilt [9]. This effect of ethanol was observed in the absence of any change in blood pressure and in spite of an increased basal heart rate [9]. In this chapter, we will discuss the acute and chronic effects of ethanol on baroreflex activity in normotensive humans and rats. Furthermore, based on our data and reported findings, we will identify the major neuroanatomical targets for ethanol action on baroreflexes and discuss a pivotal role for ethanol-evoked inhibition of glutamatergic neurotransmission in its depressant action on baroreflexes.
