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Kidney Int. 2007 Sep;72(5):566-73. Epub 2007 Jun 20.

The role of the BK channel in potassium homeostasis and flow-induced renal potassium excretion.

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Institute of Pharmacology and Toxicology, Medical Faculty of the Eberhard Karls University, Wilhelmstrasse 56, 72074 Tübingen, Germany.


The kidney is the major regulator of potassium homeostasis. In addition to the ROMK channels, large conductance Ca(2+)-activated K(+) (BK) channels are expressed in the apical membrane of the aldosterone sensitive distal nephron where they could contribute to renal K(+) secretion. We studied flow-induced K(+) secretion in BK channel alpha-subunit knockout (BK(-/-)) mice by acute pharmacologic blockade of vasopressin V(2) receptors, which caused similar diuresis in wild-type and knockout mice. However, wild-type mice, unlike the BK(-/-), had a concomitant increase in urinary K(+) excretion and a significant correlation between urinary flow rate and K(+) excretion. Both genotypes excreted similar urinary amounts of K(+) irrespective of K(+) diet. This was associated, however, with higher plasma aldosterone and stronger expression of ROMK in the apical membrane of the aldosterone-sensitive portions of the distal nephron in the knockout than in the wild-type under control diet and even more so with the high-K(+) diet. High-K(+) intake significantly increased the renal expression of the BK channel in the wild-type mouse. Finally, despite the higher plasma K(+) and aldosterone levels, BK(-/-) mice restrict urinary K(+) excretion when placed on a low-K(+) diet to the same extent as the wild-type. These studies suggest a role of the BK channel alpha-subunit in flow-induced K(+) secretion and in K(+) homeostasis. Higher aldosterone and an upregulation of ROMK may compensate for the absence of functional BK channels.

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