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Evidence for cystic fibrosis transmembrane conductance regulator-dependent sodium reabsorption in kidney, using Cftr^tm2cam mice

J. D. Kibble, A. M. Neal, W. H. Colledge*, R. Green† and C. J. Taylor‡

1. The aims of this study were to investigate (a) if renal Na⁺ handling was normal in Cftr^tm2cam F508 cystic fibrosis mice, (b) whether adaptation to dietary salt depletion was preserved and (c) whether Cftr^tm2cam F508 mice exhibited enhanced amiloride-sensitive Na⁺ absorption.

2. In Na⁺-replete animals (maintained on a 0·32 % NaCl diet) given a 150 mM NaCl i.v. maintenance infusion, there was no difference in fractional Na⁺ excretion (FE_Na) between wild-type (0·42 ± 0·06 %, n = 12) and Cftr^tm2cam F508 mice (0·47 ± 0·13 %, n = 7). Amiloride infusion significantly increased FE_Na in both wild-type (3·14 ± 0·83 %, n = 6) and Cftr^tm2cam F508 mice (3·47 ± 0·63 %, n = 9), though with no significant difference between genotypes.

3. A 14 day dietary salt restriction (animals maintained on a 0·03 % NaCl diet) and maintenance infusion with a 15 mM NaCl vehicle caused a reduction in FE_Na to 0·14 ± 0·05 %, n = 8 in wild-type mice and 0·14 ± 0·04 %, n = 8 in Cftr^tm2cam F508 mice. No significant difference in the ability to adapt to low salt conditions was apparent comparing the two genotypes.

4. Treatment of salt-restricted mice with amiloride resulted in a blunted natriuresis in both wild-type mice (FE_Na = 1·10 ± 0·16 %, n = 7) and Cftr^tm2cam F508 mice (FE_Na = 1·97 ± 0·29 %, n = 9). The natriuresis induced by amiloride was significantly greater in Cftr^tm2cam F508 mice than in wild-type controls.

5. In conclusion, Cftr^tm2cam F508 mice exhibit normal renal salt excretion when either salt replete or salt restricted. Enhanced amiloride-sensitive FE_Na is consistent with increased Na⁺ absorption via the amiloride-sensitive sodium channel ENaC, in cystic fibrosis kidney, but this was only observed during salt restriction.

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