Abstract

The i.a. administration of t-BA to perfused dog hindquarters resulted in vascular dilatation. The dilator response was not specifically inhibited by atropine or dichloroisoproterenol. Acute section of the lumbar sympathetic chains converted the dilatation to constriction. The dilator response returned when t-BA was injected during electrical stimulation of the distal sympathetic chains. Vasoconstrictor responses to electrical stimulation of the lumbar sympathetic chains are reduced by the i.a. infusion of t-BA. It is concluded that the dilator action of t-BA is dependent upon the presence of neurogenic vasoconstrictor impulses. t-BA may exert this effect by inhibiting the release of catecholamines at sympathetic nerve endings. Histamine release may also be partly responsible for the dilator response.