The role of K+ in the regulation of the increase in intracellular Ca2+ mediated by the T lymphocyte antigen receptor.
The regulation of the increase in intracellular calcium ([Ca2+]i) occurring in cytolytic T lymphocytes (CTLs) upon their interaction with antigen was examined. This [Ca2+]i increase and lytic function were insensitive to verapamil, a Ca channel blocker. An antigen-independent increase in [Ca2+]i was not induced by depolarization of CTLs with excess extracellular K+, suggesting that Ca2+ influx is not mediated by the ubiquitous voltage-gated Ca channel. The antigen-induced [Ca2+]i increase was inhibited by prior membrane hyperpolarization with valinomycin. Hyperpolarization occurred under normal circumstances in CTLs exposed to antigen-receptor-specific antibodies. This potential change was Ca2+-dependent and inhibited by K channel blockade. Conversely, K channel blockade augmented the antigen-specific [Ca2+]i increase while markedly decreasing the K+ efflux associated with CTL lytic function. Therefore, either membrane potential or intracellular K+ regulates the antigen-specific [Ca2+]i increase in CTLs.
D000818:Animals; D000941:Antigens / Q000502:physiology; D002118:Calcium / Q000502:physiology*; D002462:Cell Membrane / Q000502:physiology; D003593:Cytoplasm / Q000502:physiology; D003602:Cytotoxicity, Immunologic; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials; D051379:Mice; D011188:Potassium / Q000502:physiology*; D011948:Receptors, Antigen, T-Cell / Q000502:physiology*; D013602:T-Lymphocytes, Cytotoxic / Q000502:physiology*; D014634:Valinomycin / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D000941:Antigens; D007473:Ion Channels; D011948:Receptors, Antigen, T-Cell; D014634:Valinomycin; D014700:Verapamil; D011188:Potassium; D002118:Calcium