Nitric oxide hyperpolarizes arterial smooth muscle

M. Tare, H. C. Parkington, H. A. Coleman, T. O. Neild, G. J. Dusting

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The actions of nitric oxide (NO) on the membrane potential of vascular smooth muscle were investigated using segments of guinea pig uterine arteries that were depolarized and constricted with phenylephrine. Exogenous NO (4 x 10-8 to 4 x 10-5 M) evoked concentration-dependent hyperpolarization and relaxation that were abolished following pretreatment of the arteries with hemoglobin and methylene blue. Nitroprusside and nitroglycerine also evoked hyperpolarization and relaxation of these arteries. Inhibitors of NO synthesis, N(G)-monomethyl-L-arginine and N(ω)-nitro-L-arginine methyl ester, reduced the hyperpolarization and relaxation induced by stimulation of the endothelium with acetylcholine. These results indicate that NO, whether derived from the endothelium, the nitrovasodilators, or applied exogenously, is capable of hyperpolarizing arterial smooth muscle.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Issue numberSUPPL. 3
Publication statusPublished - 1 Jan 1991


  • Endothelium-derived relaxing factor
  • Hyperpolarization
  • N(G)-monomethyl-L-arginine
  • Nitric oxide
  • Nitrovasodilator
  • Uterine artery

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