Transmembrane potential changes associated with superoxide release from human granulocytes.
Treatment of human granulocytes with concanavalin A, phorbol myristate acetate (PMA), N-formyl-methionyl-leucyl-phenylalanine (FMLP), and A23187 (a calcium ionophore) stimulates the release of superoxide anion and the generation of chemiluminescence. The fluorescent probe, Di-S-C3(5), has been used to monitor shifts in membrane potential in response to these stimulants which precede the secretion of superoxide. Concanavalin A, PMA, and FMLP induce a biphasic shift in transmembrane potential (Em), i.e., a rapid depolarization followed by a prolonged hyperpolarization. This depolarization is dependent on both external sodium and calcium while the hyperpolarization is inhibited by ouabain which blocks the electrogenic Na-K pump. In contrast, A23187 induces a rapid and prolonged depolarization. This monophasic shift in Em is dependent on external calcium. These results suggest that depolarization acts as a signal to initiate events associated with the "respiratory burst" of these phagocytes.
D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D003208:Concanavalin A / Q000494:pharmacology; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D008564:Membrane Potentials / Q000187:drug effects; D009239:N-Formylmethionine / Q000031:analogs & derivatives / Q000494:pharmacology; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009842:Oligopeptides / Q000494:pharmacology; D010100:Oxygen / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D009842:Oligopeptides; D003208:Concanavalin A; D013481:Superoxides; D000001:Calcimycin; D009239:N-Formylmethionine; D009240:N-Formylmethionine Leucyl-Phenylalanine; D012964:Sodium; D013755:Tetradecanoylphorbol Acetate; D011188:Potassium; D010100:Oxygen; D002118:Calcium