NO- activates soluble guanylate cyclase and Kv channels to vasodilate resistance arteries
NO- activates soluble guanylate cyclase and Kv channels to vasodilate resistance arteries
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DOI:
10.1161/01.hyp.0000072010.54901.de
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发表时间:
2003-06-01
期刊:
影响因子:
8.3
通讯作者:
Kemp-Harper, BK
中科院分区:
文献类型:
--
作者:
Irvine, JC;Favaloro, JL;Kemp-Harper, BK
Nitric oxide (NO) plays an important role in the control of vascular tone. Traditionally, its vasorelaxant activity has been attributed to the free radical form of NO (NOcircle), yet the reduced form of NO (NO-) is also produced endogenously and is a potent vasodilator of large conduit arteries. The effects of NO- in the resistance vasculature remain unknown. This study examines the activity of NO- in rat small isolated mesenteric resistance-like arteries and characterizes its mechanism(s) of action. With the use of standard myographic techniques, the vasorelaxant properties of NOcircle (NO gas solution), NO- (Angeli's salt), and the NO donor sodium nitroprusside were compared. Relaxation responses to Angeli's salt (pEC(50)=7.51+/-0.13, R-max=95.5+/-1.5%) were unchanged in the presence of carboxy-PTIO (NOcircle scavenger) but those to NOcircle and sodium nitroprusside were inhibited. L-Cysteine (NO- scavenger) decreased the sensitivity to Angeli's salt (P