Upregulation of calbindin D28k in the late distal tubules in the potassium-loaded adrenalectomized mouse kidney
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Mizuka Kobayashi Yukiko Yasuoka Yuichi Sato Ming Zhou Hiroshi Abe Katsumasa Kawahara Hirotsugu Okamoto
- چاپ و سال / کشور: 2011
Description
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 andP\0.05, respectively) increased inK-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.
Clin Exp Nephrol (2011) 15:355–362 Received: 24 December 2010 / Accepted: 14 January 2011 / Published online: 24 February 2011 Japanese Society of Nephrology 2011
