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Release of catecholamines from the adrenal medulla by prostaglandin E1

1967; Elsevier BV; Volume: 2; Issue: 3 Linguagem: Inglês

10.1016/0014-2999(67)90083-0

1879-0712

S.O. Kayaalp, R. K. Türker,

Nitric Oxide and Endothelin Effects

Dogs were anesthetized with pentobarbital and their hindquarters were sympathetically denervated and autoperfused. Prostaglandin E1 was injected into the aorta at a level proximal to the arterial blood supply to the adrenal glands. As far as possible it was prevented from reaching the perfused vascular bed which served as a non-specific catecholamine detector with adequate sensitivity. Prostaglandin E1 (1–4 μg/kg) did not produce any rise but a fall in perfusion pressure when given intravenously, whereas it usually caused a sustained rise in perfusion pressure when given into the aorta. This pressor response was abolished by phenoxybenzamine or dihydroergotamine. The administration of hexamethonium a also blocked the pressor response to prostaglandin E1. The pressor response did not occur in spinal dogs or in dogs with their adrenal glands excluded from the circulation. These results indicate that prostaglandin E1 releases catecholamines from the adrenal medulla in the dog, possibly through a presynaptic action. A reflex indirect action seems to be highly unlikely.