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1 Department of Cellular and Molecular Physiology, Yale University, New Haven, Connecticut, United States
2 Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, United States
* To whom correspondence should be addressed. E-mail: ssansom{at}unmc.edu.
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.
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