Akademik Veri Yönetim Sistemi
European Journal of Pharmacology, cilt.3, sa.2, ss.139-142, 1968 (SCI-Expanded, Scopus)
Dogs were anesthetized with pentobarbital and their hindquarters were sympathetically denervated and autoperfused. Prostaglandin E1, acetylcholine and dimethylphenyl-piperazinium were injected into the aorta at a level proximal to the arterial blood supply to the adrenal glands. The drugs were prevented from reaching the perfused vascular bed as far as possible, since this served as a non-specific catecholamine detector of adequate sensitivity. Prostaglandin E1 and the two cholinergic drugs caused a rise in perfusion pressure, due to the release of catecholamines from the adrenal medulla. The pressor action of prostaglandin E1 was abolished by the intravenous administration of hemicholinium. However the latter did not affect the pressor responses to acetylcholine and dimethylphenylpiperazinium. These observations were taken as further evidence in favor of the suggestion that prostaglandin E1 releases catecholamines through a presynaptic action. The intra-aortic administration of prostaglandin E1 did not potentiate to any significant extent the release of catecholamines by the cholinergic drugs from the adrenal medulla. This makes it highly unlikely that prostaglandin E1 acts by sensitizing the chromaffin cells of the adrenal medulla to acetylcholine released at the splanchnic nerve endings, rather than by the proposed presynaptic action. © 1968.