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Am J Physiol Renal Physiol 291: F517-F529, 2006. First published June 13, 2006; doi:10.1152/ajprenal.00118.2006
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INVITED REVIEW

BK channels in the kidney: role in K+ secretion and localization of molecular components

Jennifer L. Pluznick1 and Steven C. Sansom2

1Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut; and 2Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska

Although it is generally accepted that ROMK is the K+ secretory channel in the mammalian distal nephron, recent in vitro and in vivo studies have provided evidence that large-conductance Ca2+-activated K+ channels (BK, or maxi K) also secrete K+ in renal tubules. This review assesses the current evidence relating BK channels with K+ secretion. We shall consider the component proteins of the BK channel, their localization with respect to segment and cell type, and the electrophysiological forces involved in K+ secretion. Although the majority of studies have focused on a role for BK channels in flow-mediated K+ secretion, this review also considers a potential role for BK channels in high-K diet-induced K+ secretion. The division of workload between ROMK and BK is discussed as a mechanism for ensuring a constant plasma K+ concentration.

maxi K; distal nephron; potassium secretion; connecting tubule; BK-beta1



Address for reprint requests and other correspondence: S. C. Sansom, Dept. of Cellular and Integrative Physiology, Univ. of Nebraska Medical Ctr., Omaha, NE 68198-5850 (e-mail: ssansom{at}unmc.edu)




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