Nonendothelial‐derived nitric oxide activates the ATP‐sensitive K+ channel of vascular smooth muscle cells

FEBS Letters

Nakaya, Yutaka²  Miyoshi, Hirokazu²  Moritoki, Hideki¹ 

[1] The Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, The University of Tokushima, 2-50-1, Kuramoto-cho, Tokushima City, Tokushima 770, Japan;The Second Department of Internal Medicine, School of Medicine, The University of Tokushima, 2-50-1, Kuramoto-cho, Tokushima City, Tokushima 770, Japan

关键词: Endotoxin;    ATP-sensitive K+ channel;    Nitric oxide;    Endothelium-derived hyperpolarizing factor;   

DOI  :  10.1016/0014-5793(94)00417-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

To determine whether endogenous nitric oxide (NO) opens the ATP-sensitive K⁺ channel (K_ATP channel), we investigated the effect of nonendothelial-derived NO on this channel in cultured smooth muscle cells of the porcine coronary artery by the patch-clamp technique. In the cells pretreated with endotoxin, the addition of 10⁻⁴ M l-arginine generated NO and activated the K_ATP channel. Activation of this channel was suppressed by pretreatment with 10⁻³ M N ^G-methyl-l-arginine or 10⁻³ M N ^x-nitro-l-arginine methyl ester, each of which is a specific antagonist of the l-arginine-NO pathway, and by 10⁻⁶ M Methylene blue, which blocks guanylate cyclase. The activation of the K_ATP channel by l-arginine-NO pathway is expected to produce hyperpolarization of the cell membrane and relaxation of vascular smooth muscle cells.

【 授权许可】

Unknown