Am J Physiol Cell Physiol AJP: Lung Cellular and Molecular Physiology
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Am J Physiol Cell Physiol 281: C615-C623, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 2, C615-C623, August 2001

Alterations in airway ion transport in NKCC1-deficient mice

B. R. Grubb, A. J. Pace, E. Lee, B. H. Koller, and R. C. Boucher

Cystic Fibrosis/Pulmonary Research and Treatment Center, University of North Carolina, Chapel Hill, North Carolina 27599-7248

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 (Isc) 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 Isc. 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<UP><SUB>3</SUB><SUP>−</SUP></UP> 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.

bumetanide; Na+-K+-2Cl- cotransporter; bicarbonate secretion; chloride secretion


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