{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:02:34Z","timestamp":1772895754591,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2002,4,1]]},"abstract":"<jats:p>We isolated and cultured fetal distal lung epithelial (FDLE) cells from 17- to 19-day rat fetuses and assayed for anion secretion in Ussing chambers. With symmetrical Ringer solutions, basal short-circuit currents ( I<jats:sub>sc<\/jats:sub>) and transepithelial resistances were 7.9 \u00b1 0.5 \u03bcA\/cm<jats:sup>2<\/jats:sup>and 1,018 \u00b1 73 \u03a9 \u00b7 cm<jats:sup>2<\/jats:sup>, respectively (means \u00b1 SE; n = 12). Apical amiloride (10 \u03bcM) inhibited basal I<jats:sub>sc<\/jats:sub>by \u223c50%. Subsequent addition of forskolin (10 \u03bcM) increased I<jats:sub>sc<\/jats:sub>from 3.9 \u00b1 0.63 \u03bcA\/cm<jats:sup>2<\/jats:sup>to 7.51 \u00b1 0.2 \u03bcA\/cm<jats:sup>2<\/jats:sup>( n = 12). Basolateral bumetanide (100 \u03bcM) decreased forskolin-stimulated I<jats:sub>sc<\/jats:sub>from 7.51 \u00b1 0.2 \u03bcA\/cm<jats:sup>2<\/jats:sup>to 5.62 \u00b1 0.53, whereas basolateral 4,4\u2032-dinitrostilbene-2,2\u2032-disulfonate (5 mM), an inhibitor of HCO[Formula: see text] secretion, blocked the remaining I<jats:sub>sc<\/jats:sub>. Forskolin addition evoked currents of similar fractional magnitudes in symmetrical Cl<jats:sup>\u2212<\/jats:sup>- or HCO[Formula: see text]-free solutions; however, no response was seen using HCO[Formula: see text]- and Cl<jats:sup>\u2212<\/jats:sup>-free solutions. The forskolin-stimulated I<jats:sub>sc<\/jats:sub>was inhibited by glibenclamide but not apical DIDS. Glibenclamide also blocked forskolin-induced I<jats:sub>sc<\/jats:sub>across monolayers having nystatin-permeablized basolateral membranes. Immunolocalization studies were consistent with the expression of cystic fibrosis transmembrane conductance regulator (CFTR) protein in FDLE cells. In aggregate, these findings indicate the presence of cAMP-activated Cl<jats:sup>\u2212<\/jats:sup>and HCO[Formula: see text] secretion across rat FDLE cells mediated via CFTR.<\/jats:p>","DOI":"10.1152\/ajplung.00370.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:16:38Z","timestamp":1425413798000},"page":"L650-L658","source":"Crossref","is-referenced-by-count":22,"title":["cAMP regulation of Cl<sup>\u2212<\/sup>and HCO 3 \u2212 secretion across rat fetal distal lung epithelial cells"],"prefix":"10.1152","volume":"282","author":[{"given":"Ahmed","family":"Lazrak","sequence":"first","affiliation":[{"name":"Departments of Anesthesiology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ulrich","family":"Thome","sequence":"additional","affiliation":[{"name":"Pediatrics,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carpantanto","family":"Myles","sequence":"additional","affiliation":[{"name":"Departments of 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