title: Factors responsible for acetylcholine-induced dilatation in the isolated perfused rat kidney.
abstract: Mechanism of acetylcholine (ACh)-induced dilatation was investigated in isolated perfused rat kidney. Under a constant flow of 8-10 ml/min, ACh (0.001-3 microg/0.1 ml) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine (PE). ACh-induced dilatations were inhibited by atropine (10(-6) mol/l), hexamethonium (10(-4) mol/l), indomethacin (10(-5) mol/l), methylene blue (10(-5) mol/l), N(G)-nitro-L-arginine (L-NOARG, 10(-4) mol/l), tetrodotoxin (TTX, 10(-6) mol/l), capsaicin (10(-6) mol/l), and glibenclamide (10(-5) mol/l). These results suggest that in the isolated perfused rat kidney, endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO), and tachykinin neuromediators may play a role in ACh-induced dilatation via stimulation of guanylate cyclase and opening of ATP-sensitive potassium channels.
authors: Department of Pharmacology, Faculty of Medicine, Hacettepe University, 06100, Ankara, Turkey.
authors: I
authors: I
authors: Ay
authors: S
authors: S
authors: Emre
authors: M
authors: M
authors: Tuncer
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001685:Biological Factors / Q000502:physiology*; D004106:Dilatation; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009411:Nerve Endings / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar
chemical_list: D001685:Biological Factors; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D000109:Acetylcholine