AJP - Heart and Circulatory Physiology, Vol 250, Issue 1 121-H130, Copyright © 1986 by American Physiological Society
5-Hydroxytryptamine delays relaxation time of norepinephrine-induced vasoconstriction
S. Manzini, C. A. Maggi and A. Meli
The effect of low concentration of 5-hydroxytryptamine (5-HT; 0.03-0.3
microM) on cellular and extracellular Ca2+ -dependent norepinephrine (NE; 5
microM)-induced vasoconstriction was assessed in isolated perfused rabbit
ear artery. The most remarkable effect of 5-HT is a concentration-dependent
enhancement of the duration of the extracellular Ca2+ -dependent NE-induced
vasoconstriction. This effect of 5-HT is still present in
6-hydroxydopamine-pretreated arteries and in the presence of
deoxycorticosterone and is not mimicked by the K+ channel blocker
tetraethylammonium. Administration of nifedipine (0.3 microM) and EDTA (1
mM) failed to antagonize 5-HT-induced prolongation of relaxation kinetics
of extracellular Ca2+ -dependent NE-induced vasoconstriction. On the other
hand, this phenomenon was abolished by caffeine (15 mM) and markedly
reduced by dibutyryl cyclic AMP (3 mM). 5-HT (0.3 microM), but not NE
(30-50 nM), enhanced the vasoconstriction elicited by caffeine (15 mM) that
was procaine sensitive and unaffected by nifedipine. These results suggest
that 5-HT prolonged relaxation kinetics of NE-induced vasoconstriction
through an impairment of cellular mechanisms that decrease the myoplasmic
level of free Ca2+. A similar mechanism could be of relevance for 5-HT
enhancement of vascular smooth muscle responsiveness to vasoactive agents.
