PURINE RELEASE FROM VASCULAR ADRENERGIC-NERVES BY HIGH POTASSIUM AND A CALCIUM IONOPHORE, A-23187

Abstract

The effect of high KCl and a Ca2+-ionophore, A-23187 [calcimycin], 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 .mu.M) markedly enhanced the efflux from the adrenergically innervated pulmonary artery. The KCl-induced increase of 3H-efflux was greatly diminished by removal of Ca2+ from the medium and pretreatment with 6-hydroxydopamine (30 .mu.g/ml) and cold storage (4 days) but not by treatment with reserpine and phentolamine. 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 significantly reduced by Ca2+ removal or cold storage. In the nerve-free aortic medial preparation, the efflux inducing effects of KCl and A-23187 were very limited. The remaining effect of KCl in this tissue was not Ca2+-dependent. From these results the efflux of 3H-purines induced by the high KCl or Ca2+-ionophore appears to originate mainly from the amine-containing vesicles in adrenergic nerve terminals, probably through the Ca2+-dependent exocytosis. This supports the view that the release of ATP and norepinephrine are coupled in adrenergic neurotransmission.