Trautwein W, Cavalié A, Flockerzi V, Hofmann F, Pelzer D
II. Physiologisches Institut, Universität des Saarlandes, Homburg/Saar, FRG.
Circ Res. 1987 Oct;61(4 Pt 2):I17-23.
L-type calcium channel activity of some excitable cells is markedly enhanced by beta-adrenergic agents. The enzymatic cascade underlying this important modulatory effect has been studied with patch-clamp techniques in single dialyzed ventricular cells from guinea pig heart. The steps between the binding of agonist to the beta-receptor and the increase in calcium influx can be summarized as follows: Agonist binding to beta-receptor greater than adenylate cyclase increases greater than cAMP increases greater than cA-kinase increases greater than protein phosphorylation greater than altered calcium channel properties greater than ICa increases A basal phosphorylation reaction seems not to be a prerequisite for calcium channel function. By combining molecular and functional approaches, the purified dihydropyridine-receptor complex from rabbit skeletal muscle transverse-tubules can be reconstituted in phospholipid bilayer membranes to form a functional 20-pS calcium channel that retains the principal regulatory, biochemical, and pharmacologic properties of membrane-bound L-type calcium channels.
某些可兴奋细胞的L型钙通道活性会被β-肾上腺素能药物显著增强。利用膜片钳技术，在豚鼠心脏的单个透析心室细胞中对这一重要调节作用背后的酶促级联反应进行了研究。从激动剂与β受体结合到钙内流增加之间的步骤可总结如下：激动剂与β受体结合→腺苷酸环化酶增加→环磷酸腺苷（cAMP）增加→钙激酶增加→蛋白质磷酸化→钙通道特性改变→钙电流（ICa）增加。基础磷酸化反应似乎不是钙通道功能的先决条件。通过结合分子和功能方法，可将从兔骨骼肌横管中纯化得到的二氢吡啶受体复合物重构于磷脂双层膜中，形成一个功能性的20皮安钙通道，该通道保留了膜结合L型钙通道的主要调节、生化和药理特性。
