| First Author | Grubb BR | Year | 2000 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 279 |
| Issue | 4 | Pages | G707-18 |
| PubMed ID | 11005757 | Mgi Jnum | J:65223 |
| Mgi Id | MGI:1913218 | Doi | 10.1152/ajpgi.2000.279.4.G707 |
| Citation | Grubb BR, et al. (2000) Intestinal ion transport in NKCC1-deficient mice. Am J Physiol Gastrointest Liver Physiol 279(4):G707-18 |
| abstractText | The Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) located on the basolateral membrane of intestinal epithelia has been postulated to be the major basolateral Cl(-) 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 -/- jejuna. In the -/- jejuna, the forskolin response (22 microA/cm(2); bumetanide insensitive) was significantly attenuated compared with the bumetanide-sensitive response (52 microA/cm(2)) in normal tissue. Ion-replacement studies demonstrated that the forskolin response in the NKCC1 -/- jejuna was HCO(3)(-) dependent, whereas in the normal jejuna it was independent of the HCO(3)(-) concentration in the buffer. NKCC1 -/- 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(3)(-) as well as Cl(-) entry (via non-NKCC1) paths played a role in the NKCC1 -/- secretory response. In contrast to cystic fibrosis mice, which lack both basal and stimulated Cl(-) secretion and exhibit severe intestinal pathology, the absence of intestinal pathology in NKCC1 -/- mice likely reflects the ability of the intestine to secrete HCO(3)(-) and Cl(-) by basolateral entry mechanisms independent of NKCC1. |
