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  • 标题:Modulation by calcium of the potassium permeability of dog heart sarcolemmal vesicles
  • 本地全文:下载
  • 作者:P Caroni ; E Carafoli
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:1982
  • 卷号:79
  • 期号:19
  • 页码:5763-5767
  • DOI:10.1073/pnas.79.19.5763
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:The movement of K+ in heart sarcolemmal vesicles has been followed through the opposing movement of the tetraphenylphosphonium ion. Ca2+ (5-50 microM) stimulates the efflux of K+ from K+-loaded vesicles [Km(Ca2+) approximately equal to 10 microM]. and the activation requires that Ca2+ be present inside the vesicles together with K+. The efflux of 86Rb+ from K+-, Rb+-loaded vesicles is similarly stimulated by 5-50 microM Ca2+ [Km(Ca2+) approximately equal to 10 microM]. The Ca2+-induced increase of K+ permeability does not become spontaneously inactivated. The effects of some inhibitors have been tested under conditions in which Ca2+ promotes the entry of K+ into vesicles. In this system, direct interaction of the drug with the Ca2+ and K+ membrane binding site(s) was therefore studied. Tetraethylammonium ion, which inhibits the potential-dependent K+ channel, does not interfere with the effect of Ca2+ whereas quinidine (IC50 = 12 microM) and trifluoperazine (IC50 = 8 microM at 50 micrograms of sarcolemmal protein per ml) inhibit.
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