HYPOXIA REDUCES POTASSIUM CURRENTS IN CULTURED RAT PULMONARY BUT NOT MESENTERIC ARTERIAL MYOCYTES
HYPOXIA REDUCES POTASSIUM CURRENTS IN CULTURED RAT PULMONARY BUT NOT MESENTERIC ARTERIAL MYOCYTES
复制标题
DOI：
10.1152/ajplung.1993.264.2.l116
复制
发表时间：
1993-02-01
影响因子：
--
通讯作者：
BLAUSTEIN, MP
中科院分区：
文献类型：
--
作者：
YUAN, XJ;GOLDMAN, WF;BLAUSTEIN, MP
为探讨低氧引起肺血管收缩的可能机制，采用全细胞膜片钳技术观察了低氧对原代培养的大鼠肺动脉（PA）和肠系膜动脉（MA）平滑肌细胞外向钾电流（I（out））的影响。当细胞浸泡在标准生理盐溶液中，膜片移液管含有含10 mM乙二醇-双（β-氨基乙基醚）-N，N，N '，N'-四乙酸（EGTA）的无钙培养基时，几乎所有的I（out），包括快速失活组分（I（rt））和稳态（非失活）组分（I（ss）），都是由电压门控K+通道介导的。将槽液中的O2张力从155 Torr降低至
To explore possible mechanisms underlying hypoxia-induced pulmonary vasoconstriction, the effect of hypoxia on outward K+ current (I(out)) was evaluated in primary cultured rat pulmonary (PA) and mesenteric (MA) arterial smooth muscle cells using the whole cell patch-clamp technique. When the cells were bathed in standard physiological salt solution and the patch pipettes contained Ca2+-free media with 10 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), virtually all of the I(out), including both the rapidly inactivating component (I(rt)) and the steady-state (noninactivating) component (I(ss)), was mediated by voltage-gated K+ channels. Reduction of O2 tension in the bath solution from 155 Torr to