Ik. Anderson et al., CARDIOVASCULAR EFFECTS OF SEROTONIN AND DP-5-CT IN CONSCIOUS LONG-EVANS AND BRATTLEBORO RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 40(2), 1996, pp. 455-463
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.