Transmitter release in skin and muscle blood vessels during sympathetic stimulation

Abstract

During perfusion at constant blood flow, the release of norepinephrine elicited by sympathetic nerve stimulation in the cutaneous bed of the dog''s hindpaw and gracilis muscle was determined. Stimulation in muscle caused a greater release of transmitter than stimulation in the skin as indicated by the increase in concentration and total amount of norepinephrine released into the venous effluent. The vasoconstrictor responses produced were similar in skin and muscle. An increase in blood flow in skin and muscle increased the total amount of transmitter released during stimulation, but the concentration change tended to decrease in skin and remain the same in muscle. Blockade of rebinding of norepinephrine by phenoxybenzamine resulted in a greater release into the venous effluent during stimulation in both beds. After administration of pheniprazine, a monoamine axidase inhibitor, stimulation caused a greater release of norepinephrine into the venous effluent of skin and muscle, but not if phenoxybenzamine had been given before pheniprazine. Because no evidence for greater inactivation of norepinephrine either by rebinding or metabolism by monoamine oxidase in the cutaneous bed was found, several other possible explanations were presented to explain the equivalent vasoconstrictor response in skin in the face of the sparse amount of transmitter found in the effluent.