Neurogenic release of purine compounds in blood vessels.

The isolated thoracic aorta, ear artery and portal vein of the rabbit concentrated tritiated material on exposure to tritiated adenosine, adenine and its nucleotides. 3H-adenosine was transformed and retained predominantly as 3H-adenosine triphosphate in the portal vein and aortic adventitia, but to a lesser extent in the aortic medial or muscle layer. On transmural stimulation, portal vein and aortic adventitial strips pretreated with 3H-adenosine released tritiated material, which was recovered mainly as tritiated adenosine and nucleotides. Guanethidine abolished this release in the aortic adventitia and greatly diminished it in the portal vein. Both the release and vasodilation induced by transmural stimulation in the portal vein were abolished by tetrodotoxin. It is suggested that purine compounds are released locally within vascular walls from both the adrenergic and nonadrenergic nerves. The results are compatible with the view that adenosine triphosphate or a related compound may function as an inhibitory modulator in association with the adrenergic nerves and as a vasodilator transmitter of the non-adrenergic nerves in the portal vein.