Hypoxic release of calcium from the sarcoplasmic reticulum of pulmonary artery smooth muscle

被引:118
作者
Dipp, M
Nye, PCG
Evans, AM
机构
[1] Univ Oxford, Dept Pharmacol, Oxford OX1 3QT, England
[2] Univ Oxford, Physiol Lab, Oxford OX1 3PT, England
关键词
hypoxic pulmonary vasoconstriction; ryanodine; caffeine; rabbit; isolated arteries;
D O I
10.1152/ajplung.2001.281.2.L318
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The hypoxic constriction of isolated pulmonary vessels is composed of an initial transient phase (phase 1) followed by a slowly developing increase in tone (phase 2). We investigated the roles of the endothelium and of intracellular Ca2+ stores in both preconstricted and unpreconstricted intrapulmonary rabbit arteries when challenged with hypoxia (PO2 16-21 Torr). Removing the endothelium did not affect phase 1, but phase 2 appeared as a steady plateau. Removing extracellular Ca2+ had essentially the same effect as removing the endothelium. Depletion of sarcoplasmic reticulum Ca2+ stores with caffeine and ryanodine abolished the hypoxic response. Omitting preconstriction reduced the amplitude of the hypoxic response but did not qualitatively affect any of the above responses. We conclude that hypoxia releases intracellular Ca2+ from ryanodine-sensitive stores by a mechanism intrinsic to pulmonary vascular smooth muscle without the need for Ca2+ influx across the plasmalemma or an endothelial factor. Our results also suggest that extracellular Ca2+ is required for the release of an endothelium-derived vasoconstrictor.
引用
收藏
页码:L318 / L325
页数:8
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