This study investigated the acute effects of ethanol (0.25; 0.5, or 1 g/kg, iv) on mean arterial pressure, heart rate, and gain of the baroreceptor reflex control of heart rate (BRS) in conscious spontaneously hypertensive rats (SHRs) and age-matched Wistar rats. BRS was substantially lower in the SHRs as compared with the Wistar rats when measured by phenylephrine (-0.95 +/- 0.16 vs. -2.02 +/- 0.22 beats/min/mm Hg) or nitroprusside (-1.90 +/- 0.2 vs. -3.02 +/- 0.32 beats/min/mm Hg). None of the doses of ethanol influenced BRS-in the SHR. In contrast, ethanol attenuated BRS in Wistar rats, but this effect was dependent on the dose used and the type of response. The lower doses attenuated the reflex tachycardic response, but had no effect on the refer bradycardic response. On the other hand, the 1 g/kg dose of ethanol attenuated the reflex bradycardic but not the tachycardic response. Ethanol produced a presser effect (15-25 mm Hg; 5-min duration), which was neither dose- nor strain-dependent. However, only in the SHR mean arterial pressure remained elevated (10-15 mm Hg above control) for 20 min in response to the 0.5 g/kg dose of ethanol, and its recovery coincided with the occurrence of a slowly developing negative chronotropic response. Ethanol produced a dose-related negative chronotropic effect in both strains of rats that was of longer duration in the SHR, particularly with the 1 g/kg dose. It is possible that the bradycardic effect of ethanol influenced negatively its presser effects. Data suggest that, in conscious rats, ethanol: (1) attenuates BRS in normotensive rats but not in the SHR; (2) causes a brief presser effect that is not related to its dose, the level of arterial pressure, or its influence on the gain of the baroreceptor reflex; and (3) elicits dose-related bradycardic responses that are of longer duration in the SHR, particularly with the higher dose. This negative chronotropic effect of ethanol may limit its presser effect in SHRs.