AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 2 455-R463, Copyright © 1996 by American Physiological Society
Cardiovascular effects of serotonin and DP-5-CT in conscious Long-Evans and Brattleboro rats
I. K. Anderson, A. G. Ramage and S. M. Gardiner
Department of Physiology and Pharmacology, University of Nottingham Medical School, Queen's Medical Centre, United Kingdom.
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.
