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. 2011 Jun;15(3):355-362.
doi: 10.1007/s10157-011-0414-4. Epub 2011 Feb 24.

Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney

Mizuka Kobayashi  1 , Yukiko Yasuoka  2   3 , Yuichi Sato  4 , Ming Zhou  5 , Hiroshi Abe  5 , Katsumasa Kawahara  6   7 , Hirotsugu Okamoto  1
Affiliations

Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney

Mizuka Kobayashi et al. Clin Exp Nephrol. 2011 Jun.

Abstract

Background: The calcium (Ca)-activated potassium (K) channel is an alternative K-secretory pathway in the apical membranes of the distal nephrons of adrenalectomized (ADX) animals. As a potential approach for estimating intracellular Ca(2+) increase, we investigated normal and ADX mice to determine whether dietary K intake would stimulate the expression of the calbindin D28k protein, a cytosolic Ca(2+)-binding protein, along the distal nephron consisting of the early and late portions of the distal convoluted tubule (DCT1 and DCT2, respectively), the CNT, and CCD.

Methods: ADX mice received a control diet plus either 0.3% NaCl solution (C) or a 0.3% NaCl plus 3% KCl solution (HK) for 7 days before the experiment.

Results: The mean plasma K concentration and pH were significantly (P < 0.001) higher (7.9 ± 0.3 mEq/l) and lower (7.28 ± 0.02) in the K-loaded ADX mice than in the control ADX mice. The mean urinary K excretion (mEq/day) and urine flow (ml/day) increased significantly (P < 0.0001) from 0.47 ± 0.07 (C) to 4.80 ± 0.57 (HK) and from 1.1 ± 0.2 (C) to 8.8 ± 1.0 (HK). Urinary Ca excretion significantly (P < 0.005 and P < 0.05, respectively) increased in K-loaded normal and ADX mice compared with control normal and ADX mice. Immunofluorescence studies revealed that the relative staining of calbindin was 167.0 ± 15.4%, 291.3 ± 13.8%, and 206.3 ± 11.3% for DCT1, DCT2/CNT, and CCD of normal control mice, respectively. These values increased significantly (P < 0.0001) only in DCT2/CNT (574.8 ± 42%) of the K-loaded ADX mice.

Conclusion: Upregulation of calbindin in the late distal tubule suggests that Ca(2+)-dependent K transport may function as an alternative mechanism for urinary K excretion in ADX mice.

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