Acute and chronic effects of ethanol (EOH) administration on the cardiovascular and hormonal responses to repeated hemorrhage were investigated in conscious normotensive Wistar rats and spontaneously hypertensive rats (SHR). The chronic EOH treated group received 5% EOH (vol/vol) ad libitum in the drinking water far the first week,10% for the last 2 weeks, and 20% for the last 5 weeks from the age of 6 weeks. The EOH free group received tap water. Chronic EOH and EOH free groups were randomly subdivided into acute EOH infusion and control groups. Under ether anesthesia, catheters were inserted into the femoral vein and both femoral arteries. After rats regained consciousness and their blood pressure was stabilized, responses to quick hemorrhage (5 ml/kg BW) were tested. In the acute EOH infusion group, hemorrhage was induced 20 min after EOH infusion (1.0 g/kg BW), Baroreceptor reflex sensitivity was assessed by the ratio of changes in hen.1 rate and mean arterial pressure (ΔHR/ΔMAP) immediately after the hemorrhage. Chronic EOH administration elevated MAP in Wistar rats. During acute EOH infusion, MAP do- creased and HR increased in all groups. In comparison to EOH free control rats, acute or chronic EOH treated rats showed a greater reduction in MAP and a smaller elevation in heart rate in response to a hemorrhage. The degree of MAP reduction was significantly greater in SHR than in Wistar rats. Both the acute and chronic EOH administration attenuated the baroreceptor reflex and retarded MAP recovery, again the trend being much more prominent in SHR. The increase in plasma vasopressin and lenin concentrations after hemorrhage were intensified by the chronic EOH administration. SHR showed a greater vasopressin response but a smaller lenin response than Wistar rats. These results indicate that the EOH treated rats, particularly SHB, are prone to shock by a hemorrhage, which may be partly attributed to an impaired baroreceptor reflex function.