Serotonergic vasoconstriction in human fingers during reflex sympathetic response to cooling
Coffman, J.D.; Cohen, R.A.
American Journal of Physiology 254(5 Pt 2): H889-H893
1988
ISSN/ISBN: 0002-9513 PMID: 3364592 Document Number: 313106
The effect on finger blood flow (FBF) of 5-hydroxytryptamine (5-HT) in a 25.degree. C room and the S2-serotonergic receptor antagonist, ketanserin, during reflex smpathetic vasoconstriction was studied in normal subjects. Total FBF was measured by venous occlusion, air plethysmography, and capillary blood flow (FCF) by the disappearance rate of a radiosotope from a fingertip injection. 5-HT in doses of 4 and 8 .mu.g/ml, given by constant infusion via a brachial artery catheter, significantly decreased FBF [32 .+-. (SE) 10.4 to 12.8 .+-. 6.6 for 4 .mu.g/ml and to 5.4 .+-. 2.6 ml .cntdot. min-1 .cntdot. 100 ml-1 for 8 .mu.g/min, P < 0.05]. Ketanserin (50 .mu.g/min) blocked the vasoconstriction caused by 5-HT. During reflex sympathetic vasoconstriction produced by body cooling, ketanserin increased FBF from 4.1 .+-. 1.1 to 39.9 .+-. 12.9 ml .cntdot. min1 .cntdot. 100 ml-1 (P < 0.025). The vasodilation caused by ketanserin was specific for serotonergic receptors, since it occurred during .alpha.1-adrenoceptor blockade with prazosin. Furthermore, the decreases in FBF induced by clonidine and angiotensin II were not significantly different before and during ketanserin infusion. Also, ketanserin further increased FBF after vasodilation of reflexly vasoconstricted fingers by the .alpha.2-adrenoceptor antagonist, yohimbine, and phentolamine increased FBF during ketanserin infusions. FCF decreased during 5-HT and increased during ketanserin infusions, demonstrating that both capillary and arteriovenous shunt flow were affected. Vasoconstriction of the finger caused by body cooling appears to be mediated by both .alpha.2-adrenergic and serotonergic mechanisms. S2-serotonergic receptors are present in the human finger and are activated by 5-HT during reflex sympathetic vasoconstriction.