{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:50:07Z","timestamp":1772164207107,"version":"3.50.1"},"reference-count":47,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,7,1]]},"abstract":"<jats:p>\n                    In cortical collecting ducts (CCDs) perfused in vitro, inhibiting the epithelial Na\n                    <jats:sup>+<\/jats:sup>\n                    channel (ENaC) reduces Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption. Since ENaC does not transport Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    , the purpose of this study was to determine how ENaC modulates Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption. Thus, Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption was measured in CCDs perfused in vitro that were taken from mice given aldosterone for 7 days. In wild-type mice, we observed no effect of luminal hydrochlorothiazide on either Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption or transepithelial voltage ( V\n                    <jats:sub>T<\/jats:sub>\n                    ). However, application of an ENaC inhibitor [benzamil (3 \u03bcM)] to the luminal fluid or application of a Na\n                    <jats:sup>+<\/jats:sup>\n                    -K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase inhibitor to the bath reduced Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption by \u223c66\u201375% and nearly obliterated lumen-negative V\n                    <jats:sub>T<\/jats:sub>\n                    . In contrast, ENaC inhibition had no effect in CCDs from collecting duct-specific ENaC-null mice (Hoxb7:CRE, Scnn1a\n                    <jats:sup>loxlox<\/jats:sup>\n                    ). Whereas benzamil-sensitive Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption did not depend on CFTR, application of a Na\n                    <jats:sup>+<\/jats:sup>\n                    -K\n                    <jats:sup>+<\/jats:sup>\n                    -2Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    cotransport inhibitor (bumetanide) to the bath or ablation of the gene encoding Na\n                    <jats:sup>+<\/jats:sup>\n                    -K\n                    <jats:sup>+<\/jats:sup>\n                    -2Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    cotransporter 1 (NKCC1) blunted benzamil-sensitive Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption, although the benzamil-sensitive component of V\n                    <jats:sub>T<\/jats:sub>\n                    was unaffected. In conclusion, first, in CCDs from aldosterone-treated mice, most Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption is benzamil sensitive, whereas thiazide-sensitive Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption is undetectable. Second, benzamil-sensitive Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    absorption occurs by inhibition of ENaC, possibly due to elimination of lumen-negative V\n                    <jats:sub>T<\/jats:sub>\n                    . Finally, benzamil-sensitive Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    flux occurs, at least in part, through transcellular transport through a pathway that depends on NKCC1.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00030.2012","type":"journal-article","created":{"date-parts":[[2012,4,12]],"date-time":"2012-04-12T00:34:09Z","timestamp":1334190849000},"page":"F45-F55","source":"Crossref","is-referenced-by-count":27,"title":["ENaC inhibition stimulates Cl\n                    <sup>\u2212<\/sup>\n                    secretion in the mouse cortical collecting duct through an NKCC1-dependent mechanism"],"prefix":"10.1152","volume":"303","author":[{"given":"Vladimir","family":"Pech","sequence":"first","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monika","family":"Thumova","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Young Hee","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diana","family":"Agazatian","sequence":"additional","affiliation":[{"name":"Department of Medicine, Emory University School of Medicine, Atlanta, Georgia;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edith","family":"Hummler","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bernard 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