title: Alkaline pH and internal calcium increase Na+ and K+ effluxes in LK sheep red blood cells in Cl--free solutions.
abstract: We examined the effects of pH, internal ionized Ca (Ca2+i), cellular ATP, external divalent cations and quinine on Cl-independent ouabain-resistant K+ efflux in volume-clamped sheep red blood cells (SRBCs) of normal high (HK) and low (LK) intracellular K+ phenotypes. In LK SRBCs the K+ efflux was higher at pH 9.0 (350%) than at pHs 7. 4 and 6.5, and was inhibited by external divalent cations, quinine, and cellular ATP depletion. The above findings suggest that the increased K+ efflux at alkaline pH is due to the opening of ion channels or specific transporters in the cell membrane. In addition, K+ efflux was activated (100%) when Ca2+i was increased (+A23187, +Ca2+o) into the microm range. However, in comparison to human red blood cells, the Ca2+i-induced increase in K+ efflux in LK SRBCs was fourfold smaller and insensitive to quinine and charybdotoxin. The Na+ efflux was also higher at pH 9.0 than at pH 7.4, and activated (about 40%) by increasing Ca2+i. In contrast, in HK SRBCs the K+ efflux at pH 9.0 was neither inhibited by quinine nor activated by Ca2+i. These studies suggest the presence in LK SRBCs, of at least two pathways for Cl--independent K+ and Na+ transport, of which one is unmasked by alkalinization, and the other by a rise in Ca2+i.
authors.affiliation: Department of Physiology and Biophysics, Wright State University, Dayton, OH 45401-0927, USA.
authors.forename: O
authors.initials: O
authors.lastname: Ortiz-Carranza
authors.forename: M E
authors.initials: ME
authors.lastname: Miller
authors.forename: N C
authors.initials: NC
authors.lastname: Adragna
authors.forename: P K
authors.initials: PK
authors.lastname: Lauf
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects* / Q000378:metabolism; D002413:Cations, Divalent / Q000494:pharmacology; D018999:Charybdotoxin / Q000494:pharmacology; D002712:Chlorides; D004912:Erythrocytes / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D017136:Ion Transport / Q000187:drug effects; D007476:Ionophores / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D011803:Quinine / Q000494:pharmacology; D012756:Sheep / Q000097:blood; D012964:Sodium / Q000378:metabolism*
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002413:Cations, Divalent; D002712:Chlorides; D007476:Ionophores; D018999:Charybdotoxin; D000001:Calcimycin; D000255:Adenosine Triphosphate; D012964:Sodium; D011803:Quinine; D011188:Potassium; D002118:Calcium