Serotonergic vasoconstriction in human fingers during reflex sympathetic response to cooling.

The effect on finger blood flow (FBF) of 5-hydroxytryptamine (5-HT) in a 25 degrees C room and the S2-serotonergic receptor antagonist, ketanserin, during reflex sympathetic 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 radioisotope from a fingertip injection. 5-HT in doses of 4 and 8 micrograms/min, given by constant infusion via a brachial artery catheter, significantly decreased FBF [32 +/- (SE) 10.4 to 12.8 +/- 6.6 for 4 micrograms/min and to 5.4 +/- 2.6 ml.min-1.100 ml-1 for 8 micrograms/min, P less than 0.05]. Ketanserin (50 micrograms/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.min-1.100 ml-1 (P less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)