Purine release from vascular adrenergic nerves by high potassium and a calcium ionophore, A-23187.

The effect of high KCl and a Ca++-ionophore, A-23187, on 3H-purine efflux from [3H]adenosine-labeled pulmonary artery and thoracic aortic media of the rabbit was assessed. High KCl (30, 50 and 70 mM) and A-23187 (5 microM) markedly enhanced the efflux from the adrenergically innervated pulmonary artery. The KCl-induced increase of 3H-efflux was greatly diminished by removal of Ca++ from the medium and pretreatment with 6-hydroxydopamine (30 micrograms/ml) and cold storage (4 days), but not by treatment with reserpine and phentolamine. In contrast, the 3H-efflux induced by l-epinephrine was not affected by cold storage or 6-hydroxydopamine but was inhibited by phentolamine. 3H-purine efflux by A-23187 was also significantly reduced by Ca++ removal or cold storage. In the nerve-free aortic medial preparation, the efflux inducing effects of both KCl and A-23187 were very limited. The remaining effect of KCl in this tissue was not Ca++-dependent. From these results the efflux of 3H-purines induced by the high KCl or Ca++-ionophore appears to originate mainly from the amine-containing vesicles in adrenergic nerve terminals, probably through the Ca++-dependent exocytosis. This supports the view that the release of ATP and norepinephrine are coupled in adrenergic neurotransmission.