| 11845319 |
Chan LN, Wang XF, Tsang LL, So SC, Chung YW, Liu CQ, Chan HC: Inhibition of amiloride-sensitive Na (+) absorption by activation of CFTR in mouse endometrial epithelium. Pflugers Arch. 2001;443 Suppl 1:S132-6. Epub 2001 Jul 10.
Previous studies have demonstrated amiloride-sensitive Na (+) absorption under basal conditions and cystic fibrosis transmembrane conductance regulator (CFTR)-mediated Cl (-) secretion following neurohormonal stimulation in the mouse endometrial epithelium. The present study investigated the inhibition of amiloride-sensitive Na (+) absorption accompanying activation of CFTR in the mouse endometrium using the short-circuit current ( I (sc)) technique. RT-PCR demonstrated the co-expression of CFTR and epithelial Na (+) channels (ENaC) in primary cultured mouse endometrial epithelia and cultured endometrial monolayers exhibited a basal amiloride-sensitive I (sc) of 5.4 +/- 0.6 microA/cm (2). The amiloride-sensitive current fell to 3.1 +/- 0.5 microA/cm (2) after stimulation with forskolin. When the possible contribution of Na (+) absorption to the I (sc) was eliminated by amiloride (1 microM) or Na (+) replacement, the forskolin-induced I (sc) was not reduced, but rather increased significantly compared with that in the absence of amiloride or in Na (+)-containing solutions ( P < 0.02), indicating that the forskolin-induced I (sc) was mediated by Cl (-) secretion, portion of which may be masked by concurrent inhibition of basal Na (+) absorption if the contribution of Na (+) is not eliminated. When the contribution of Cl (-) to the I (sc) was eliminated by diphenylamine 2,2'-dicarboxylic acid (DPC, 2 mM) or Cl (-) replacement, forskolin now decreased, rather than increased the I (sc), demonstrating the inhibition of Na (+) absorption upon stimulation. Our data suggest an interaction between CFTR and ENaC, which may be the underlying mechanism for balancing Na (+) absorption and Cl (-) secretion across the mouse endometrial epithelium. |
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