| First Author | Grubb BR | Year | 2001 |
| Journal | Am J Physiol Cell Physiol | Volume | 281 |
| Issue | 2 | Pages | C615-23 |
| PubMed ID | 11443061 | Mgi Jnum | J:70873 |
| Mgi Id | MGI:2148412 | Doi | 10.1152/ajpcell.2001.281.2.C615 |
| Citation | Grubb BR, et al. (2001) Alterations in airway ion transport in NKCC1-deficient mice. Am J Physiol Cell Physiol 281(2):C615-23 |
| abstractText | Airways of Na(+)-K(+)-2Cl(-) (NKCC1)-deficient mice (-/-) were studied in Ussing chambers to determine the role of the basolateral NKCC1 in transepithelial anion secretion. The basal short-circuit current (I(sc)) of tracheae and bronchi from adult mice did not differ between NKCC1-/- and normal mice, whereas NKCC1-/- tracheae from neonatal mice exhibited a significantly reduced basal I(sc). In normal mouse tracheae, sensitivity to the NKCC1 inhibitor bumetanide correlated inversely with the age of the mouse. In contrast, tracheae from NKCC1-/- mice at all ages were insensitive to bumetanide. The anion secretory response to forskolin did not differ between normal and NKCC1-/- tissues. However, when larger anion secretory responses were induced with UTP, airways from the NKCC1-/- mice exhibited an attenuated response. Ion substitution and drug treatment protocols suggested that HCO secretion compensated for reduced Cl(-) secretion in NKCC1-/- airway epithelia. The absence of spontaneous airway disease or pathology in airways from the NKCC1-/- mice suggests that the NKCC1 mutant mice are able to compensate adequately for absence of the NKCC1 protein. |
