Involvement of calcium in calcium-current inactivation in smooth muscle cells from rat vas deferens.
Ca-channel currents were recorded in Cs-loaded single smooth muscle cells from rat vas deferens to define the dependence of the inactivation time course on Ca concentration. The decay of Ca-channel current obtained in a Ba2+- or Sr2+-containing external solution during long voltage-clamp pulses was much slower than that in a Ca-containing solution. The difference was not due to a change in the surface potential of the membrane as judged from the steady-state activation and inactivation curves. When Ca was the charge carrier, increasing external Ca concentration slightly accelerated the rate of inactivation. In addition, the rate of inactivation of Ca-channel current in 10.8 mM Ba was also accelerated by adding Ca to the external solution in a concentration-dependent manner. The time course of Ca-current inactivation was slowed when the cells were dialyzed with a high concentration of citrate, a Ca-chelating agent. From these results, we concluded that a mechanism regulated by intracellular Ca activity plays a role in the inactivation of Ca channels in smooth muscle. The Ca-dependent process may protect against Ca overload by regulating Ca entry in smooth muscle cells.
D000818:Animals; D001464:Barium; D002118:Calcium / Q000502:physiology*; D002951:Citrates / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D004553:Electric Conductivity; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology*; D007700:Kinetics; D008297:Male; D009130:Muscle, Smooth / Q000502:physiology*; D051381:Rats; D013324:Strontium; D014649:Vas Deferens / Q000502:physiology*
D002951:Citrates; D007473:Ion Channels; D001464:Barium; D004533:Egtazic Acid; D002118:Calcium; D013324:Strontium