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   <subfield code="a">Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Mizuka Kobayashi, Yukiko Yasuoka, Yuichi Sato, Ming Zhou, Hiroshi Abe, Katsumasa Kawahara, Hirotsugu Okamoto]</subfield>
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   <subfield code="a">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 7days before the experiment. Results: The mean plasma K concentration and pH were significantly (P&lt;0.001) higher (7.9±0.3mEq/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&lt;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&lt;0.005 and P&lt;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&lt;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.</subfield>
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   <subfield code="a">Japanese Society of Nephrology, 2011</subfield>
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   <subfield code="a">Hyperkalemia</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hyperchloremic metabolic acidosis</subfield>
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   <subfield code="a">Hypercalciuria</subfield>
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   <subfield code="a">Ca2+-dependent K excretion in distal tubule</subfield>
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   <subfield code="a">Kobayashi</subfield>
   <subfield code="D">Mizuka</subfield>
   <subfield code="u">Department of Anesthesiology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, 252-0374, Sagamihara, Japan</subfield>
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   <subfield code="a">Yasuoka</subfield>
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   <subfield code="u">Department of Cellular and Molecular Physiology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, 252-0374, Sagamihara, Japan</subfield>
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   <subfield code="u">Department of Applied Tumor Pathology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, Sagamihara, Japan</subfield>
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   <subfield code="u">Department of Cellular and Molecular Physiology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, 252-0374, Sagamihara, Japan</subfield>
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   <subfield code="u">Department of Anesthesiology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, 252-0374, Sagamihara, Japan</subfield>
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