beta-Adrenoceptor agonist accelerates recovery from inactivation of calcium-dependent action potentials.

The voltage-activated Ca2+ channel in cardiac muscle plasma membranes is regulated by beta-adrenoceptor agonist, presumably by cyclic AMP-dependent phosphorylation of membrane proteins associated with this channel. In chick ventricle, we find that isoproterenol accelerates the recovery from inactivation of the maximum rate of rise (Vmax) of Ca2+-dependent action potentials without changing the steady-state inactivation of Vmax. These results confirm and extend those of others who found that beta-adrenoceptor agonists accelerated the repriming kinetics of bullfrog atrial Ca2+ current (iCa) channels. Patch clamp experiments showed that beta-adrenoceptor agonists change the kinetics of iCa channels so as to increase the probability that an iCa channel is available to open, primarily by reducing the intervals between bursts of channel openings. It is concluded that the altered kinetics of iCa channel repriming caused by beta-adrenoceptor agonist in multicellular preparations is consistent with the action of these drugs in increasing the probability of channel opening and the time spent in the open state.