{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T22:48:30Z","timestamp":1774565310822,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1995,4,1]]},"abstract":"<jats:p> We investigated cation transport and cell volume regulation in erythrocytes of CD1 and C57\/B6 mice. Swelling of cells from either strain stimulated K+ efflux that was insensitive to ouabain, bumetanide, and clotrimazole. Seventy-five percent of swelling-induced K+ efflux was Cl- dependent (inhibited by sulfamate or methanesulfonate, partially by NO3-, but not by SCN-) and was inhibited by okadaic acid (OA; 50% inhibitory concentration = 18 +\/- 6 nM in CD1 and 10 +\/- 4 nM in C57\/B6). In both strains, K+ efflux into isotonic medium was stimulated by staurosporine or by N-ethylmaleimide, and the latter was partially blocked by pretreatment of cells with OA. When cells of either strain were incubated in hypotonic medium or preswollen isosmotically with nystatin, OA-sensitive regulatory volume decrease (RVD) and K+ loss were observed. RVD produced by hypotonic swelling was prevented by Cl- replacement with sulfamate or methanesulfonate. These properties suggest the presence in outbred and inbred mouse erythrocytes of RVD mediated by K(+)-Cl- cotransport. <\/jats:p>","DOI":"10.1152\/ajpcell.1995.268.4.c894","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T18:39:42Z","timestamp":1514140782000},"page":"C894-C902","source":"Crossref","is-referenced-by-count":50,"title":["Cation transport in mouse erythrocytes: role of K(+)-Cl- cotransport in regulatory volume decrease"],"prefix":"10.1152","volume":"268","author":[{"given":"C. C.","family":"Armsby","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, Children's Hospital, Boston,Massachusetts, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Brugnara","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Children's Hospital, Boston,Massachusetts, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. L.","family":"Alper","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Children's Hospital, Boston,Massachusetts, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Cell Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajpcell.1995.268.4.C894","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:37:25Z","timestamp":1718653045000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajpcell.1995.268.4.C894"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1995,4,1]]}},"alternative-id":["10.1152\/ajpcell.1995.268.4.C894"],"URL":"https:\/\/doi.org\/10.1152\/ajpcell.1995.268.4.c894","relation":{},"ISSN":["0363-6143","1522-1563"],"issn-type":[{"value":"0363-6143","type":"print"},{"value":"1522-1563","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,4,1]]}}}