CARDIOVASCULAR EFFECTS OF SEROTONIN AND DP-5-CT IN CONSCIOUS LONG-EVANS AND BRATTLEBORO RATS

The regional hemodynamic changes caused by intracerebroventricular 5-h ydroxytryptamine (5-HT) were investigated in conscious Long-Evans and Brattleboro rats with chronically implanted Doppler flow probes. In bo th strains, a low dose of 5-HT (4 nmol/kg) caused a presser response a ssociated with tachycardia, mesenteric vasoconstriction, and a transie nt hindquarters vasodilatation. In Long-Evans rats, higher doses of 5- HT (40 and 120 nmol/kg) caused a presser response, a bradycardia, mese nteric vasoconstriction, and maintained hindquarters dilatation. The b radycardia and mesenteric vasoconstriction caused by 40 nmol/kg of 5-H T in Long-Evans rats were attenuated by d(CH2)(5)Tyr(Me)arginine vasop ressin, a V-1-receptor antagonist. In Brattleboro rats the high doses of 5-HT failed to cause a presser response but caused a delayed depres sor response, a transient tachycardia, less mesenteric vasoconstrictio n, and a larger initial hindquarters dilatation compared with Long-Eva ns rats. The initial part of the hindquarters vasodilator response cau sed by 120 nmol/kg of 5-HT in Brattleboro rats was attenuated by the b eta(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 icy), a 5-HT1A receptor agonist, caused a tachycardia associated w ith a marked hindquarters vasodilatation. These changes were accompani ed by a weak mesenteric vasoconstriction and, for the highest dose of DP-5-CT, a presser response. These data overall are consistent with th e hemodynamic effects of intracerebroventricular 5-HT contingent on va sopressin release and, along with DP-5-CT, sympathoadrenal excitation; however, additional mechanisms are indicated.