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

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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 Ca2+ increase, we investigated normal and ADX mice to determine whether dietary K intake would stimulate the expression of the calbindin D28k protein, a cytosolic Ca2+-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 Ca2+-dependent K transport may function as an alternative mechanism for urinary K excretion in ADX mice.

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Acknowledgments

This study was supported by grants from Research Projects of the Kitasato University GSMS to K. K. (2008, 2009) and H. K. (2006, 2007) and from The Salt Science Research Foundation (nos. 0635, 0727). We thank Dr. H. Nonoguchi (Hyogo College Med., Nephrology) for providing helpful comments. Special thanks are extended to Y. Nakabayashi for her technical assistance. Parts of this study were presented at the meetings of the ISN/Nexus 2010 (Kyoto). The Kidney and Vascular System: Emerging Culprits in Pathogenesis and Advances in Therapy (p102) and The XXXVI IUPS 2009 (Kyoto) (J Physiol Sci 2009; 59 (Suppl): 485). Pacific Edit reviewed the manuscript before submission.

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Correspondence to Katsumasa Kawahara.

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M. Kobayashi and Y. Yasuoka contributed equally to this work.

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Kobayashi, M., Yasuoka, Y., Sato, Y. et al. Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney. Clin Exp Nephrol 15, 355–362 (2011). https://doi.org/10.1007/s10157-011-0414-4

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  • DOI: https://doi.org/10.1007/s10157-011-0414-4

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