Montiel C, Artalejo A R, García A G
Biochem Biophys Res Commun. 1984 May 16;120(3):851-7. doi: 10.1016/s0006-291x(84)80185-0.
Reintroduction of Ca ions to cat adrenal glands perfused at room temperature with Krebs solution lacking Ca and Mg, evoked a catecholamine secretory response that was directly proportional to the concentration of Ca reintroduced. This secretory response inactivated quickly, was abolished by nM concentrations of nifedipine and was potentiated dramatically by nM concentrations of BAY-K-8644. Excess Ca antagonized the inhibitory effects of nifedipine and this drug inhibited competitively the potentiating effects of BAY-K-8644. These data suggest 1st) that extracellular divalent cations deprivation activates specific Ca channels; 2nd) that the dihydropyridine BAY-K-8644 increases the release of catecholamines by Ca reintroduction by activating and/or delaying the inactivation of Ca channels; and 3rd) that the access of the dihydropyridine-type Ca agonist and antagonists to their "intra-channel" site of action requires the pre-activation of Ca channels.
将钙离子重新引入在室温下用不含钙和镁的 Krebs 溶液灌注的猫肾上腺，会引发儿茶酚胺分泌反应，该反应与重新引入的钙浓度成正比。这种分泌反应迅速失活，纳摩尔浓度的硝苯地平可将其消除，而纳摩尔浓度的 BAY-K-8644 可使其显著增强。过量的钙可拮抗硝苯地平的抑制作用，且该药物竞争性抑制 BAY-K-8644 的增强作用。这些数据表明：第一，细胞外二价阳离子剥夺可激活特定的钙通道；第二，二氢吡啶类药物 BAY-K-8644 通过激活和/或延迟钙通道失活，增加了钙重新引入时儿茶酚胺的释放；第三，二氢吡啶类钙激动剂和拮抗剂进入其“通道内”作用位点需要钙通道预先激活。
