Role of alpha-adrenoceptor subtypes mediating sympathetic vasoconstriction in human digits

Abstract. The effects of intra-arterial administration of alpha-1 and alpha-2 adrenoceptor agonists and antagonists on human digital blood flow were studied before and during reflex sympathetic vasoconstriction in normal subjects. Total finger flow was measured by venous occlusion air plethysmography and capillary flow by the disappearance rate of a radioisotope from a local injection in a fingerpad. Intra-arterial phenylephrine (0·2–1·3 μg min^-1) and clonidine (0·12–0·48 μg min^-1) produced dose-related decreases in finger blood flow and increases in vascular resistance. Clonidine was the more potent vasoconstrictor. Prazosin (0·48 μg min^-1) effectively blocked the vasoconstrictor effect of phenylephrine but not clonidine, while yohimbine (30–70 μg min^-1) blocked the effect of clonidine but not phenylephrine. In a 20°C room, prazosin (0·4–13·2 μg min^-1) caused no significant changes in finger blood flow (7·7 ± 2·1 to 11·7 ± 3·3 ml min^-1) 100 ml^-1) or vascular resistance (30·9 ± 8·8 to 28·1 ± 8·7 mmHg ml^-1 min^-1 100 ml^-1). In the 20°C room, yohimbine (30–70 μg min^-1) produced a significant increase in finger blood flow (7·8 ± 2·8 to 23·4 ± 6·8 ml, P>0·01) and decrease in vascular resistance (20·5 ± 5·7 to 6·0 ± 2·2 units, P>0·01). No significant changes occurred in finger capillary flow with prazosin or yohimbine infusions. It is concluded that alpha-1 and alpha-2 adrenoceptors are present in human digital vasculature and that alpha-2 adrenoceptors are more important than alpha-1 adrenoceptors in sympathetic neural vasoconstriction. Since capillary blood flow was unaffected by yohimbine infusions during reflex sympathetic vasoconstriction, the alpha-2 adrenoceptors predominantly influence arteriovenous shunts in the finger.