Beta-adrenergic vasodilator mechanism in the finger.

Abstract

The digital vasospastic phenomena, which are induced by beta-adrenergic-blocking agents, suggest a beta-adrenergic finger vasodilator mechanism. We measured fingertip total blood flow with venous occlusion plethysmography and studied nutritional blood flow with Na131I clearance. During fingertip vasoconstriction caused by branchial artery infusion of norepinephrine or angiotensin, intra-arterial isoproterenol caused a sustained increase in fingertip total blood flow. Furthermore, propranolol significantly potentiated the vasoconstriction caused by intra-arterial norepinephrine and attenuated the vasodilator action of isoproterenol. No change in branchial artery blood pressure occurred to explain the changes in fingertip blood flow. Isoproterenol did not change nutritional flow, implying beta-adrenergic vasodilation solely of the fingertip arteriovenous shunts. When fingertip vasoconstriction was induced by reflex sympathetic nerve action during environmental cooling and mental stress, or by norepinephrine release from sympathetic nerves caused by intra-arterial tyramine infusion, isoproterenol and propranolol had no effect on fingertip total blood flow. This effect is probably specific for the beta-receptor agonist, since intra-arterial histamine caused a large increase in finger blood flow during environmental cooling. We conclude that there is a beta-adrenergic vasodilator mechanism in human digital arteriovenous shunts that may be humorally activated, but which has no apparent functional role in modulating sympathetic vasoconstriction. Our results suggest a spatial dissociation of the effector sites for vasoactive humoral agents and sympathetic vasoconstrictor nerves.