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

作者：Kobayashi Mizuka; Yasuoka Yukiko; Sato Yuichi; Zhou Ming; Abe Hiroshi; Kawahara Katsumasa^*; Okamoto Hirotsugu

来源：Clinical and Experimental Nephrology, 2011, 15(3): 355-362.

DOI：10.1007/s10157-011-0414-4

• Hyperkalemia
• Hyperchloremic metabolic acidosis
• Hypercalciuria
• Ca2+-dependent K excretion in distal tubule

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.
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.
The mean plasma K concentration and pH were significantly (P < 0.001) higher (7.9 +/- A 0.3 mEq/l) and lower (7.28 +/- A 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 +/- A 0.07 (C) to 4.80 +/- A 0.57 (HK) and from 1.1 +/- A 0.2 (C) to 8.8 +/- A 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 +/- A 15.4%, 291.3 +/- A 13.8%, and 206.3 +/- A 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 +/- A 42%) of the K-loaded ADX mice.
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.

• 出版日期2011-6