期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 464, 期 2-3, 页码 101-109出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-2999(03)01427-4
关键词
hydrogen peroxide; hyperpolarization; ATP-sensitive K+ channel; prostaglandin; smooth muscle vascular
The effects of H2O2 on the membrane potential of smooth muscle cells of rabbit mesenteric resistance arteries were investigated. H2O2 (3-30 muM) concentration-dependently hyperpolarized the membrane; this was inhibited by catalase but not by superoxide dismutase or the hydroxyl-radical scavenger dimethylthiourea. The cyclooxygenase inhibitor diclofenac partly inhibited the responses; the subsequent addition of the 5-lipoxygenase inhibitor 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (AA-861) (but not the cytochrome P-450 inhibitor 17-octadecynoic acid) further attenuated H2O2-induced hyperpolarizations. The sarcolemmal ATP-sensitive K+ (K-ATP) channel inhibitor 1-{5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenylsulfonyl}-3-methylthiourea, sodium salt (HMR-1098), blocked the H2O2-induced hyperpolarization in the absence and presence of diclofenac. H2O2 increased the production of prostaglandin E-2 and prostacyclin (estimated from its stable metabolite 6-keto-prostaglandin F-1alpha), both of which produce a HMR-1098-sensitive hyperpolarization in the smooth muscle cells. It is concluded that, in smooth muscle cells of rabbit mesenteric artery, H2O2 increases the synthesis of vasodilator prostaglandins and possibly 5-lipoxygenase products, which produce a hyperpolarization by activating sarcolemmal K-ATP channels. (C) 2003 Elsevier Science B.V All rights reserved.
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