{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T06:32:38Z","timestamp":1776753158692,"version":"3.51.2"},"reference-count":30,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2000,10,1]]},"abstract":"<jats:p>The Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup>cotransporter (NKCC1) located on the basolateral membrane of intestinal epithelia has been postulated to be the major basolateral Cl<jats:sup>\u2212<\/jats:sup>entry pathway. With targeted mutagenesis, mice deficient in the NKCC1 protein were generated. The basal short-circuit current did not differ between normal and NKCC1 \u2212\/\u2212 jejuna. In the \u2212\/\u2212 jejuna, the forskolin response (22 \u03bcA\/cm<jats:sup>2<\/jats:sup>; bumetanide insensitive) was significantly attenuated compared with the bumetanide-sensitive response (52 \u03bcA\/cm<jats:sup>2<\/jats:sup>) in normal tissue. Ion-replacement studies demonstrated that the forskolin response in the NKCC1 \u2212\/\u2212 jejuna was HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>dependent, whereas in the normal jejuna it was independent of the HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>concentration in the buffer. NKCC1 \u2212\/\u2212 ceca exhibited a forskolin response that did not differ significantly from that of normal ceca, but unlike that of normal ceca, was bumetanide insensitive. Ion-substitution studies suggested that basolateral HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>as well as Cl<jats:sup>\u2212<\/jats:sup>entry (via non-NKCC1) paths played a role in the NKCC1 \u2212\/\u2212 secretory response. In contrast to cystic fibrosis mice, which lack both basal and stimulated Cl<jats:sup>\u2212<\/jats:sup>secretion and exhibit severe intestinal pathology, the absence of intestinal pathology in NKCC1 \u2212\/\u2212 mice likely reflects the ability of the intestine to secrete HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>and Cl<jats:sup>\u2212<\/jats:sup>by basolateral entry mechanisms independent of NKCC1.<\/jats:p>","DOI":"10.1152\/ajpgi.2000.279.4.g707","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T15:26:36Z","timestamp":1514129196000},"page":"G707-G718","source":"Crossref","is-referenced-by-count":47,"title":["Intestinal ion transport in NKCC1-deficient mice"],"prefix":"10.1152","volume":"279","author":[{"given":"B. 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