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Kcnmb4−/− mice have decreased tubular dilation under high urinary flow

Our laboratory has shown that with volume expansion, flow through the tubules increased by 10‐fold as Na and water reabsorption was inhibited. How the renal tubules accommodate the very large increases in tubular flow has never been answered. We propose that during high tubular flow, tubular cross‐sectional area (CA) is increased by reducing the size of the cells lining the nephron. The large‐conductance, calcium‐activated K channels (BK) can play a role in cell volume regulation. Furthermore, BK are expressed in several nephron segments including the thick ascending limb (TAL), distal convoluted tubule (DCT), connecting tubule (CNT), and cortical collecting duct (CCD). We placed wild type (WT) and BK‐β4−/− (Kcnmb4−/−) mice on a normal (0.6% K) or K‐adapted (5% K or KA) diet for 10 days and measured tubular CA of the proximal tubule (PCT), TAL, CNT, and CCD. Immunohistochemical analysis with segment specific antibodies revealed that KA mice had significantly increased CA of all tubular segments compared to phenotype matched controls on a normal diet. However, the CA of the TAL, CNT, and CCD of the KA Kcnmb4−/− were significantly less than that of the KA WT mice (TAL: 174.4 vs 203.3; CNT: 278.1 vs 444.0; CCD: 901.6 vs 1401.0 μm2) indicating an inability of the Kcnmb4−/− tubules to fully dilate. No edema was present in the KA kidneys. These results reveal that increased flow leads to tubular dilation by a BK‐β4 dependent mechanism. Supported by NIH/NIDDK grant R01DK71014 (SCS).