Properties of smooth muscle hyperpolarization and relaxation to K+ in the rat isolated mesenteric artery

• Published in: American journal of physiology. Heart and circulatory physiology 2001-06, Vol.280 (6), p.H2424-H2429
• Main Authors: Dora, Kim A, Garland, Christopher J
• Format: Article
• Language: English
• Subjects: Acetylcholine - pharmacology; Animals; Barium - pharmacology; Biological Factors - metabolism; Biological Factors - pharmacology; Dose-Response Relationship, Drug; Enzyme Inhibitors - pharmacology; In Vitro Techniques; Male; Membrane Potentials - drug effects; Membrane Potentials - physiology; Mesenteric Artery, Superior - drug effects; Mesenteric Artery, Superior - metabolism; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - metabolism; NG-Nitroarginine Methyl Ester - pharmacology; Ouabain - pharmacology; Phenylephrine - pharmacology; Potassium - metabolism; Potassium - pharmacology; Rats; Vasoconstrictor Agents - pharmacology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2001.280.6.h2424

Department of Pharmacy and Pharmacology, University of Bath, Bath BA2 7AY, United Kingdom Smooth muscle membrane potential and tension in rat isolated small mesenteric arteries (inner diameter 100-200 µm) were measured simultaneously to investigate whether the intensity of smooth muscle stimulation and the endothelium influence responses to exogenous K + . Variable smooth muscle depolarization and contraction were stimulated by titration with 0.1-10 µM phenylephrine. Raising external K + to 10.8 mM evoked correlated, sustained hyperpolarization and relaxation, both of which were inhibited as the smooth muscle depolarized and contracted to around 38 mV and 10 mN, respectively. At these higher levels of stimulation, raising the K + concentration to 13.8 mM still hyperpolarized and relaxed the smooth muscle. Relaxation to endothelium-derived hyperpolarizing factor, released by ACh, was not altered by the level of stimulation. In endothelium-denuded arteries, the concentration-relaxation curve to K + was shifted to the right but was not depressed. In denuded arteries, relaxation to K + was unaffected by the extent of prior stimulation and was blocked with 0.1 mM ouabain but not with 30 µM Ba 2+ . The ability of K + to stimulate simultaneous hyperpolarization and relaxation in the mesenteric artery is consistent with a role as an endothelium-derived hyperpolarizing factor activating inwardly rectifying K + channels on the endothelium and Na + -K + -ATPase on the smooth muscle cells. endothelium-derived hyperpolarizing factor; membrane potential; acetylcholine; vascular smooth muscle