title: Release of the free nitric oxide radical (NO) and EDRF from endothelial cells.
abstract: Release of nitric oxide (NO) from cultured macrovascular endothelial cells (EC) and from isolated perfused guinea pig hearts was measured with a specific spectrophotometric assay. Under basal conditions NO was continuously released from cultured cells and from isolated hearts into the coronary effluent perfusate. Bradykinin (10(-7) M) increased rate of NO release maximally two- to three-fold in both experimental models. Onset of NO release always preceded start of vasodilation (less than 15 s). Our results provide evidence that under basal and bradykinin-stimulated conditions. 1) endothelial cells release nitric oxide as a free radical, 2) NO is solely responsible for the vasodilatory properties of EDRF and, 3) under in vivo conditions the endogenous formation of NO is quantitatively sufficient to influence the coronary vascular tone and thus, may play an important role in the regulation of coronary vascular resistance.
authors.affiliation: Institut für Physiologie I, Medizinische Einrichtungen der Heinrich-Heine-Universität Düsseldorf, FRG.
authors.forename: M
authors.initials: M
authors.lastname: Kelm
authors.forename: M
authors.initials: M
authors.lastname: Feelisch
authors.forename: J
authors.initials: J
authors.lastname: Schrader
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology; D001920:Bradykinin / Q000494:pharmacology; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D005609:Free Radicals; D006168:Guinea Pigs; D009569:Nitric Oxide / Q000378:metabolism*; D010477:Perfusion; D013552:Swine; D014664:Vasodilation / Q000502:physiology
chemical_list: D005609:Free Radicals; D009569:Nitric Oxide; D001920:Bradykinin