Inward rectifier potassium channels in the rat middle cerebral artery.
Inward rectifier potassium channels in the rat middle cerebral artery.
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大鼠大脑中动脉的内向整流钾通道。
DOI：
10.1152/ajpregu.1998.274.2.r541
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
BryanJr,RM
中科院分区：
文献类型：
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作者：
Johnson,TD;Marrelli,SP;Steenberg,ML;Childres,WF;BryanJr,RM
研究了离体大鼠大脑中动脉（MCA）向内整流K+通道（Kirs）。向腔外液中加入15mm K+(KCl)使MCAs扩张。这些扩张被Kirs的选择性抑制剂（40 μM BaCl2or 40 mM CsCl）阻断，但对其他K+通道（格列本脲、四乙基铵或4-氨基吡啶）没有选择性抑制剂阻断。内皮去除和一氧化氮合酶抑制剂（ng -硝基精氨酸甲酯，10 μM）均不影响K+诱导的血管扩张。在静息MCAs中加入bacl2会产生8-12%的剂量依赖性收缩，这表明在静息条件下，Kirs有助于设定或决定静息张力。在40-100 mmHg范围内，加入K+产生的扩张或bac2产生的收缩的大小与压力无关。我们得出结论，Kirs存在于大鼠MCA血管平滑肌上，当激活时产生扩张。这些Kirs有助于确定血管的静息张力，它们的功能与生理压力范围内的压力无关。
Inward rectifier K+channels (Kirs) were studied in the isolated perfused rat middle cerebral artery (MCA). The addition of 15 mM K+(KCl) to the extraluminal bath dilated the MCAs. These dilations were blocked by selective inhibitors for the Kirs (40 μM BaCl2or 40 mM CsCl) but not selective inhibitors for other K+channels (glibenclamide, tetraethylammonium, or 4-aminopyridine). Neither removal of the endothelium nor treatment with the nitric oxide synthase inhibitor (NG-nitro-l-arginine methyl ester, 10 μM) affected the K+-induced dilation. The addition of BaCl2to resting MCAs produced a dose-dependent constriction of 8–12%, indicating that, during resting conditions, Kirs aid in setting or determining the resting tone. The magnitude of the dilations produced by the addition of K+or constrictions produced by BaCl2were independent of pressure over a range of 40–100 mmHg. We conclude that Kirs, which produce a dilation when activated, exist on the vascular smooth muscle of the rat MCA. These Kirs aid in determining the resting tone of the vessel, and their function is independent of pressure over physiological pressure ranges.