Flow-mediated NO release from endothelial cells is independent of K+ channel activation or intracellular Ca2+.
Flow-mediated NO release from endothelial cells is independent of K+ channel activation or intracellular Ca2+.
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内皮细胞流介导的 NO 释放不依赖于 K 通道激活或细胞内 Ca2+。
DOI：
10.1152/ajpcell.1995.269.4.c863
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
O'Neill,WC
中科院分区：
文献类型：
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作者：
O'Neill,WC
在培养的牛主动脉内皮细胞中研究了 K+ 通道和细胞内 [Ca2+] 在流诱导的一氧化氮 (NO) 产生中的作用。在胶原蛋白包被的微载体珠上生长并灌注在柱中的细胞中测量 NO 释放（以亚硝酸盐产生量测量）和 K+ 通道活性（以 86Rb+ 流出量测量）。流量增加八倍会导致 NO 释放快速（1 分钟内）、持续且可逆地增加六倍。 86Rb+ 的流出量也增加，但很快回到基线，然后当流量减少时短暂减少。这可能是由于边界层冲刷而不是 K+ 通道激活，因为[3H]哇巴因的释放观察到相同的模式。四乙铵和阻断 K+ 电流的增加介质 [K+] 都不能阻止水流诱导的 NO 释放。去除培养基中的 Ca2+ 或螯合细胞内的 Ca2+ 也不会阻止流动介导的 NO 释放。结果表明，流量快速增加内皮细胞的 NO 释放，但 NO 释放的增加并不依赖于 K+ 通道的激活或细胞内 [Ca2+] 的变化。
The role of K+ channels and intracellular [Ca2+] in flow-induced nitric oxide (NO) production was investigated in bovine aortic endothelial cells in culture. NO release (measured as nitrite production) and K+ channel activity (measured as 86Rb+ efflux) were measured in cells grown on collagen-coated microcarrier beads and perfused in a column. An eightfold increase in flow produced a rapid (within 1 min), sustained, and reversible sixfold increase in NO release. Efflux of 86Rb+ also increased but rapidly returned to baseline and then transiently decreased when flow was decreased. This was probably due to boundary layer washout rather than to K+ channel activation, because an identical pattern was seen for release of [3H]ouabain. Neither tetraethylammonium nor increasing medium [K+] to block K+ currents prevented flow-induced NO release. Removal of medium Ca2+ or chelation of intracellular Ca2+ also did not block flow-mediated NO release. The results demonstrate that flow rapidly increases NO release from endothelial cells but that this increase in NO release is not dependent on activation of K+ channels or changes in intracellular [Ca2+].