Modulation of calcium channel function by phosphorylation in guinea pig ventricular cells and phospholipid bilayer membranes.
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.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004095:Dihydropyridines / Q000378:metabolism; D006168:Guinea Pigs; D006352:Heart Ventricles; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D008051:Lipid Bilayers / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D010743:Phospholipids; D010766:Phosphorylation; D011955:Receptors, Drug / Q000378:metabolism; D013566:Sympathomimetics / Q000494:pharmacology
D004095:Dihydropyridines; D007473:Ion Channels; D008051:Lipid Bilayers; D010743:Phospholipids; D011955:Receptors, Drug; D013566:Sympathomimetics; D002118:Calcium