The cardiovascular effects of centrally administered carbachol were examined in conscious Long-Evans (LE) and Brattleboro (DI) rats. Carbachol induced a long-lasting increase in blood pressure and a decrease in heart rate in LE rats, whereas in DI rats no bradycardia was observed and the pressor response was significantly less than that in Long-Evans rats. Intravenous vasopressin antagonist, d(CH₂)₅ Tyr(Me)AVP, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol in LE rats. However, the pressor response to carbachol in DI rats was still significantly less than that in LE rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in LE rats and completely eliminated it in DI rats. These results suggest that hypertensive response to i.c.v. carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by an increase in circulating vasopressin.