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Am J Physiol Renal Physiol (March 4, 2003). doi:10.1152/ajprenal.00010.2003
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Submitted on January 9, 2003
Accepted on February 26, 2003

Renal Fluid and Electrolyte Handling in BKCa-{beta}1-/- Mice

Jennifer L. Pluznick1, Peilin Wei1, Pamela K. Carmines1, and Steven C. Sansom1*

1 Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, NE, USA

* To whom correspondence should be addressed. E-mail: ssansom{at}unmc.edu.

Large-conductance Ca2+-activated K+ channels (BKCa) are comprised of pore-forming {alpha} subunits and one of four accessory {beta} subunits. The {beta}1 subunit, found predominantly in smooth muscle, modulates the Ca2+-sensitivity and pharmacological properties of BKCa. BKCa-{beta}1 null mice (M{beta}1-/-) are moderately hypertensive, consistent with the role of BKCa to modulate intrinsic vascular tone. Because BKCa are present in various renal cells including the mesangium and cortical collecting ducts, we determined if fluid or electrolyte excretion was impaired in M{beta}1-/- under euvolemic, volume expanded, or high salt diet conditions. Under euvolemic conditions, no differences in renal function were found between M{beta}1-/- and M{beta}1+/+. However, GFR and fractional K+ excretion were significantly impaired in M{beta}1-/- in response to acute volume expansion. In contrast, M{beta}1-/- exhibited enhanced Na+ excretion and fractional Na+ excretion responses to acute volume expansion. Differences in renal function between M{beta}1+/+ and M{beta}1-/- were not observed when chronically treated with a high salt diet. These observations indicate that the {beta}1 subunit of BKCa contributes to the increased GFR that accompanies an acute salt and volume load, and raises the possibility that it is also involved in regulating K+ excretion under these conditions.




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