Beta-adrenergic modulation of the slow gating process of cardiac calcium channels.
Single Ca channel currents were recorded from isolated guinea pig ventricular myocytes in the presence of 50 mM Ba by the patch clamp technique under cell-attached configuration. When a constant short depolarizing pulse was applied repetitively, a single Ca channel opened in bursts during some depolarizing steps but completely failed to open in other steps. The opening probability of Ca channels in current-containing sweeps was little affected by adrenaline. There was a tendency for either failure, or success, in inducing a burst, to occur in clusters. The histogram of the number of successes between two failures showed a single exponential distribution with a time constant of 1-2 sec in controls and 2-4 sec in the presence of adrenaline (2 X 10(-6) M). The mean number of failures between two successes was diminished considerably by adrenaline. In ventricular myocytes adrenaline seems to increase the Ca current mainly by decreasing the rate of the Ca channel for the transition between one mode at which the channel is allowed to open on depolarization and other modes.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology; D006168:Guinea Pigs; D006329:Heart Conduction System / Q000187:drug effects* / Q000502:physiology; D006352:Heart Ventricles / Q000187:drug effects; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects* / Q000502:physiology; D016276:Ventricular Function
D000318:Adrenergic beta-Agonists; D007473:Ion Channels; D004837:Epinephrine