SUMMARY We studied the effect of 12 weeks of ethanol feeding on arterial blood pressure and baroreceptor reflex control of heart rate in Sprague-Dawley and Wistar rats. Baroreceptor reflex sensitivity and pressor responsiveness were evaluated by evoking graded rises in mean arterial pressure with increasing doses of phenylephrine and angiotensin II. After 12 weeks of ethanol feeding there was a modest increase in mean arterial pressure with no change in heart rate in both strains. When angiotensin II or phenylephrine was used as the pressor agent, baroreceptor reflex curves (relationships between changes in mean arterial pressure and heart rate) of Wistar rats were shifted upward and had a markedly reduced slope compared with those of control rats, suggesting that impairment of baroreceptor reflex control of heart rate had occurred. This effect was less evident in the Sprague-Dawley rats. Ethanol-fed rats had a higher sympathetic activity, since /3-blockade with propranolol decreased heart rate to a greater degree than that seen in control rats. The pressor response curve of phenylephrine was shifted to the right in control rats challenged with ethanol (0.5 g/kg), implying the presence of a-blockade. This shift was not present in ethanol-fed rats, showing that tolerance had developed to this effect of ethanol. These findings show that attenuation of baroreceptor reflex function is associated with ethanol-induced hypertension but do not establish whether this is a cause or an effect of the developed hypertension. (Hypertension 10: 67-73, 1987) KEY WORDS • ethanoi • hypertension • baroreceptors • heart rate phenylephrine • cardiac /3-blockade • sympathetic activity N UMEROUS epidemiological studies have established that there is a positive correlation between the duration and extent of ethanol intake and the development of hypertension.1 " 3 Recent controlled clinical trials have shown that ethanol acts as a pressor agent, even in hypertensive patients, 4 and that when ethanol intake ceases blood pressure returns to predrinking levels. 45 However, whether ethanol is the causative agent cannot be determined from such studies. Similarly, the mechanism (or mechanisms) by which ethanol intake elevates blood pressure is unknown, probably because of the absence of a satisfactory animal model.Recently, Chan and Sutter and colleagues 6 ' 7 developed a rat model for ethanol-induced hypertension in which they showed that ethanol intake for 4 to 12 weeks caused a moderate rise in blood pressure. After 12 weeks of ethanol feeding, elevated blood pressure