Vascular potassium channels mediate oxygen-induced pulmonary vasodilation in fetal lambs.
Vascular potassium channels mediate oxygen-induced pulmonary vasodilation in fetal lambs.
复制标题
血管钾通道介导胎羔中氧诱导的肺血管舒张。
DOI：
10.1159/000014196
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Konduri,GG
中科院分区：
文献类型：
--
作者：
Mital,S;Konduri,GG
The pulmonary vascular resistance decreases at birth secondary to release of endothelium-derived nitric oxide (EDNO). EDNO release is a calcium-dependent process, and endothelial potassium (K+) channels regulate intracellular calcium flux. We investigated the hypothesis that potassium channels mediate oxygen-induced pulmonary vasodilation and EDNO release in fetal lambs. We instrumented 18 near-term fetal lambs at 122–126 days of gestation to measure pulmonary pressures, flow, and resistance. We studied hemodynamic effects of (1) 100% oxygen; (2) pinacidil, an ATP-sensitive K+(KATP) channel agonist, and (3) S-nitroso-N-acetylpenicillamine (SNAP), a NO donor. We studied the effects of glybenclamide, a KATPchannel antagonist, tetraethylammonium chloride (TEA), a preferential KCachannel antagonist, and nitro-L-arginine (NLA), an NO synthase inhibitor, on the response to some of the above agents. Oxygen-induced pulmonary vasodilation was inhibited by both glybenclamide and TEA, indicating that KATPand KCachannels mediate pulmonary vasodilator response to oxygen. Blocking NO synthesis with NLA inhibited pinacidil-mediated pulmonary vasodilation, indicating that KATPchannel activation stimulates NO release. SNAP-mediated pulmonary vasodilation was inhibited by TEA, but not glybenclamide, indicating that KCachannels, but not KATPchannels, mediate effects of NO on vascular smooth muscle relaxation. In conclusion, K+channels mediate oxygen-induced pulmonary vasodilation in fetal lambs. KATPchannels appear to mediate EDNO release, while KCachannels probably mediate NO effects on vascular smooth muscle.
