Electrical stimulation causes endothelium-dependent relaxation in lung vessels.
Ring segments of blood vessels were isolated from the lungs of rabbits, cats, and monkeys. After constriction with norepinephrine, electrical field stimulation caused smooth muscle relaxation in these segments. Mechanical removal of the endothelial layer, verified by scanning electron microscopy, abolished or greatly attenuated the relaxation. The response could be restored in part by apposing the endothelial surface of another vessel segment and the denuded inner surface of the constricted vessel segment. Incubation with tetrodotoxin, procaine hydrochloride, guanethidine, propranolol, atropine, metiamide, indomethacin, quinacrine hydrochloride, 5,8,11,14-eicosatetraynoic acid, aminophylline, and verapamil failed to block or enhance the relaxation response to field stimulation. We conclude that the vascular endothelium in the larger pulmonary arteries and veins studied contains a diffusible substance that inhibits smooth muscle contraction. Its release by electrical field stimulation in vitro does not involve classic neuronal transmitter release or metabolism of arachidonic acid by cyclooxygenase or lipooxygenase.
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004558:Electric Stimulation; D004727:Endothelium / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D007545:Isoproterenol / Q000494:pharmacology; D007700:Kinetics; D008168:Lung / Q000502:physiology*; D008855:Microscopy, Electron, Scanning; D009638:Norepinephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011652:Pulmonary Circulation / Q000187:drug effects; D011817:Rabbits; D013779:Tetrodotoxin / Q000494:pharmacology
D013779:Tetrodotoxin; D001285:Atropine; D011433:Propranolol; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine