title: Nitric oxide induced membrane hyperpolarization in the rat aorta is not mediated by glibenclamide-sensitive potassium channels.
abstract: Using conventional intracellular microelectrode techniques, the membrane potential (Em) of vascular smooth muscle cells in isolated segments of thoracic rat aorta was measured. The influence of exogenous and of endothelium-derived nitric oxide on the Em was assessed, and the involvement of glibenclamide-sensitive channels in the observed membrane hyperpolarization was investigated. Exposures of the aorta strips to sodium nitroprusside (10(-8)-10(-5) M) caused a concentration-dependent and endothelium-independent hyperpolarization. Maximal hyperpolarization (5.7 +/- 0.4 mV) was obtained with 10(-5) M sodium nitroprusside. Acetylcholine (10(-8)-10(-5) M produced endothelium-dependent hyperpolarizations. At low concentrations, a slow Em change was elicited, which was sustained in the presence of the vasodilator. Higher concentrations of acetylcholine caused hyperpolarizations consisting of an initial transient peak followed by a more sustained component. Pre-exposure to Ng-nitro-L-arginine (L-NNA, 2 x 10(-4) M), which depolarized Em by 2.5 +/- 0.7 mV, significantly attenuated the later component of hyperpolarizations, indicating that it is NO dependent. Glibenclamide (10-5 M) did not significantly affect the hyperpolarization induced by 10(-6)-10(-5) M sodium nitroprusside nor the maintained component of hyperpolarization induced by 10(-5) M acetylcholine. It is concluded that the hyperpolarization caused by exogenous or endogenous NO in the rat aorta is not mediated by activation of glibenclamide-sensitive potassium channels.
authors.affiliation: Department of Physiology and Physiopathology, University of Gent, Belgium. Bert.Vanheel@rug.ac.be
authors.forename: B
authors.initials: B
authors.lastname: Vanheel
authors.forename: J
authors.initials: J
authors.lastname: Van de Voorde
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism / Q000494:pharmacology*; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D007004:Hypoglycemic Agents; D015221:Potassium Channels; D014665:Vasodilator Agents; D009599:Nitroprusside; D019335:Nitroarginine; D009569:Nitric Oxide; D005905:Glyburide