Alpha-adrenergic and serotonergic mechanisms in the human digit.

The effects of intra-arterial administration of alpha 1- and alpha 2-adrenoceptor and S2-serotonergic agonists and antagonists on human digital blood flow were studied before and during reflex sympathetic vasoconstriction caused by body cooling in normal subjects. Total finger blood flow (FBF) was measured by venous occlusion plethysmography and capillary blood flow (FCF) by the disappearance rate of a radioisotope from a local injection in a fingerpad. Intra-arterial phenylephrine and clonidine produced dose-related decreases in FBF and increases in finger vascular resistance (FVR); clonidine was the more potent vasoconstrictor. Prazosin effectively blocked the vasoconstrictor effect of phenylephrine but not clonidine and yet caused no significant change in FBF and FVR during reflex sympathetic vasoconstriction. Yohimbine blocked the effect of clonidine but not phenylephrine and caused a significant increase in FBF and decrease in FVR during vasoconstriction. No significant changes occurred in FCF with prazosin or yohimbine. 5-Hydroxytryptamine decreased FBF and increased FVR. The S2-serotonergic antagonist, ketanserin, blocked the effects of 5-hydroxytryptamine. Ketanserin, in the presence of prazosin, significantly increased FBF and decreased FVR in the reflex vasoconstricted subjects. These studies suggest that both alpha 1- and alpha 2-adrenoceptors are present in the digital vascular bed and that sympathetic nerves control the flow through arteriovenous anastomoses primarily by alpha 2-adrenoceptors. S2-serotonergic receptors are also present in the digital vasculature and may be another important mechanism mediating digital vasoconstriction.