Palade P
J Biol Chem. 1987 May 5;262(13):6142-8.
Calcium ions that have been preloaded into isolated sarcoplasmic reticulum subfractions in the presence of ATP and pyrophosphate may be released upon addition of a large number of diverse pharmacologic substances. We report here that not only caffeine, but also Ca2+ ions, thymol, quercetin, menthol, halothane, chloroform, 1-ethyl-2-methylbenzimidazole, ryanodine, tetraphenylboron, ketoconazole, miconazole, clotrimazole, W-7, doxorubicin, 5,5'-dithiobis-(2-nitrobenzoic acid), p-chloromercuribenzoic acid, and low concentrations of Ag+ induce Ca2+ release from such triadic sarcoplasmic reticulum. All these drugs induce increased undirectional Ca2+ efflux. We believe all these drug-induced Ca2+ releases are mediated by Ca2+ efflux through the same ion channel since these releases are all greatly attenuated when light sarcoplasmic reticulum is substituted for triads and are even more pronounced when transverse tubule-free terminal cisternae are substituted for triads, and all these forms of drug-induced Ca2+ release are inhibited by submicromolar concentrations of ruthenium red, and by submillimolar concentrations of tetracaine, 9-aminoacridine, and Ba2+, yet they are not affected by nifedipine even at a concentration of 50 microM.
在ATP和焦磷酸存在的情况下预加载到分离的肌浆网亚组分中的钙离子，在添加大量不同的药理物质后可能会释放出来。我们在此报告，不仅咖啡因，而且Ca2+离子、百里酚、槲皮素、薄荷醇、氟烷、氯仿、1-乙基-2-甲基苯并咪唑、ryanodine、四苯基硼、酮康唑、咪康唑、克霉唑、W-7、阿霉素、5,5'-二硫代双-(2-硝基苯甲酸)、对氯汞苯甲酸以及低浓度的Ag+都会诱导这种三联体肌浆网释放Ca2+。所有这些药物都会诱导单向Ca2+外流增加。我们认为所有这些药物诱导的Ca2+释放都是通过同一个离子通道介导的Ca2+外流，因为当用轻肌浆网替代三联体时，这些释放都会大大减弱，而当用无横管的终池替代三联体时，这种减弱甚至更明显，并且所有这些形式的药物诱导的Ca2+释放都受到亚微摩尔浓度的钌红以及亚毫摩尔浓度的丁卡因、9-氨基吖啶和Ba2+的抑制，但即使在50微摩尔的浓度下，它们也不受硝苯地平的影响。
