title: Ca(2+)-activated K+ channel and the activation of Ca2+ influx in vanadate-treated red blood cells.
abstract: The mechanism by which K+ inhibits vanadate-induced 45Ca2+ influx by human red blood cells (RBC) was studied using several independent approaches. The following results were found: 1. The inhibitory effect of K+ was absent when RBC were loaded with a Ca(2+)-chelator. This treatment at the same time inhibited the vanadate-induced K+ efflux, and the membrane hyperpolarization induced by Ca2+ in vanadate-treated cells. 2. The potency of K+, Rb+, and Cs+ to inhibit vanadate-induced Ca2+ influx corresponded to their ability to depolarize the RBC membrane via the Ca(2+)-activated K+ channel (K(Ca)). 3. Inhibition of the vanadate-induced 45Ca2+ influx by a protonophore proceeded in parallel with the inhibition of the vanadate-plus-Ca(2+)-induced membrane hyperpolarization. 4. Valinomycin in part released the inhibition of the vanadate-induced Ca2+ influx by known K(Ca) inhibitors (quinine, oligomycin, 4-aminopyridine) but not by inhibitors of the Ca2+ channel (Cu2+, HS-reagents, organic Ca2+ channel blockers). 5. K+ did not inhibit the vanadate-induced Ca2+ influx in dog RBC which have K(Ca) but no transmembrane K+ gradient. The inhibition of the vanadate-induced Ca2+ influx by external K+ appears to be due to the elimination of the electrical component of the Ca(2+)-motive force imposed by opening of the K(Ca). This implies that the Ca2+ carrier mediating the influx of Ca2+ in the presence of vanadate is of uniport type, and that the activity of K(Ca) may serve as a supporting element for Ca2+ influx.
authors.affiliation: Department of Biochemistry and Microbiology, Slovak University of Technology, Bratislava, Slovakia. varecka@checdek.chtf.stuba.sk
authors.forename: L
authors.initials: L
authors.lastname: Varecka
authors.forename: E
authors.initials: E
authors.lastname: Peterajová
authors.forename: J
authors.initials: J
authors.lastname: Sevcík
mesh_terms: D000634:Aminoquinolines / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000097:blood*; D002614:Chelating Agents / Q000494:pharmacology; D004285:Dogs; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000187:drug effects* / Q000378:metabolism*; D012458:Salicylanilides / Q000494:pharmacology; D014475:Uncoupling Agents / Q000494:pharmacology; D014634:Valinomycin / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology*
chemical_list: D000634:Aminoquinolines; D002614:Chelating Agents; D015221:Potassium Channels; D012458:Salicylanilides; D014475:Uncoupling Agents; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D014634:Valinomycin; D014638:Vanadates; D004533:Egtazic Acid; C035738:Quin2-acetoxymethyl ester; C003390:3,3',4',5-tetrachlorosalicylanilide; D011188:Potassium; D002118:Calcium