Bonnet P, Vandier C, Cheliakine C, Garnier D
Laboratoire d'Electrophysiologie et de Pharmacologie Cellulaires (CNRS EP 21), Université de Tours, France.
Exp Physiol. 1994 Jul;79(4):597-600. doi: 10.1113/expphysiol.1994.sp003793.
Severe hypoxia (< 10 mmHg) induced relaxation of precontracted rings obtained from large diameter (3-4 mm) pulmonary arteries of the rabbit but had no effect upon their basal tone nor upon the length of enzymatically isolated smooth muscle cells. In isolated smooth muscle cells severe hypoxia increased a voltage-gated K+ current. The magnitude of this response depended upon the degree of intracellular Ca2+ buffering, being abolished by 10 mM EGTA. The hypoxic response of K+ currents demonstrates a direct effect of hypoxia on pulmonary artery smooth muscle cells via a modulation of potassium channel activity.
严重缺氧（<10 mmHg）可使取自兔大口径（3 - 4 mm）肺动脉的预收缩环舒张，但对其基础张力及酶分离的平滑肌细胞长度均无影响。在分离的平滑肌细胞中，严重缺氧可增加电压门控钾电流。该反应的幅度取决于细胞内钙缓冲程度，10 mM乙二醇双四乙酸（EGTA）可消除此反应。钾电流的缺氧反应表明，缺氧通过调节钾通道活性对肺动脉平滑肌细胞产生直接影响。
