The regional hemodynamic changes caused by intracerebroventricular 5-hydroxytryptamine (5-HT) were investigated in conscious Long-Evans and Brattleboro rats with chronically implanted Doppler flow probes. In both strains, a low dose of 5-HT (4 nmol/kg) caused a pressor response associated with tachycardia, mesenteric vasoconstriction, and a transient hindquarters vasodilatation. In Long-Evans rats, higher doses of 5-HT (40 and 120 nmol/kg) caused a pressor response, a bradycardia, mesenteric vasoconstriction, and maintained hindquarters dilatation. The bradycardia and mesenteric vasoconstriction caused by 40 nmol/kg of 5-HT in Long-Evans rats were attenuated by d(CH2)5Tyr(Me)arginine vasopressin, a V1-receptor antagonist. In Brattleboro rats the high doses of 5-HT failed to cause a pressor response but caused a delayed depressor response, a transient tachycardia, less mesenteric vasoconstriction, and a larger initial hindquarters dilatation compared with Long-Evans rats. The initial part of the hindquarters vasodilator response caused by 120 nmol/kg of 5-HT in Brattleboro rats was attenuated by the beta 2-adrenoceptor antagonist ICI-118551. In Long-Evans rats, N,N-di-n-propyl-5-carboxamidotryptamine maleate (DP-5-CT; 3, 30, and 100 nmol/kg icv), a 5-HT1A receptor agonist, caused a tachycardia associated with a marked hindquarters vasodilatation. These changes were accompanied by a weak mesenteric vasoconstriction and, for the highest dose of DP-5-CT, a pressor response. These data overall are consistent with the hemodynamic effects of intracerebroventricular 5-HT contingent on vasopressin release and, along with DP-5-CT, sympathoadrenal excitation; however, additional mechanisms are indicated.