Endothelium-derived vascular relaxing factor.

摘要: A large number and variety of compounds (acetylcholine, adenosine diphosphate, triphosphate, arachidonic acid, bradykinin, Ca2+ ionophores, calcitonin gene-related peptide, histamine, hydralazine, substance P, thrombin, vasoactive intestinal polypeptide) have been shown to relax arterial smooth muscle indirectly. The endothelium in muscular arteries from several species appears receptors for these vasodilators. Binding one its endothelial results the release (and presumably synthesis) substance(s) that act on cause relaxation. name endothelium-derived relaxing factor (EDRF) has proposed or substances responsible inhibition contraction. Studies determine additivity endothelium-dependent agents sensitivity EDRF-mediated responses a inhibitors suggest single common mechanism induces relaxation vascular muscle. Pharmacological studies equivocal with regard postulated involvement phospholipases acid suggestion EDRF is an oxidative, non-cyclooxygenase product arachidonate. Experiments transfer reversal consistently indicate quite labile. There convincing evidence activates guanylate cyclase, which increase intracellular cyclic guanosine 3',5'-monophosphate levels. stimulation cyclase by provides valuable sensitive parameter as well cells culture. At present, identity role cardiovascular homeostasis are unknown.