Inhibition of dihydropyridine-sensitive calcium entry in hypoxic relaxation of airway smooth muscle.
Inhibition of dihydropyridine-sensitive calcium entry in hypoxic relaxation of airway smooth muscle.
复制标题
气道平滑肌缺氧松弛过程中二氢吡啶敏感钙进入的抑制。
DOI：
10.1152/ajplung.1995.268.2.l201
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Hirshman,CA
中科院分区：
文献类型：
--
作者：
Vannier,C;Croxton,TL;Farley,LS;Hirshman,CA
Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.
