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1Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; and 2Division of Pediatric Nephrology, Department of Pediatrics, Mount Sinai School of Medicine, New York, New York
Submitted 10 February 2005 ; accepted in final form 16 May 2005
The cortical collecting duct (CCD) is a final site for regulation of K+ homeostasis. CCD K+ secretion is determined by the electrochemical gradient and apical permeability to K+. Conducting secretory K+ (SK/ROMK) and maxi-K channels are present in the apical membrane of the CCD, the former in principal cells and the latter in both principal and intercalated cells. Whereas SK channels mediate baseline K+ secretion, maxi-K channels appear to participate in flow-stimulated K+ secretion. Chronic dietary K+ loading enhances the CCD K+ secretory capacity due, in part, to an increase in SK channel density (Palmer et al., J Gen Physiol 104: 693710, 1994). Long-term exposure of Ambystoma tigrinum to elevated K+ increases renal K+ excretion due to an increase in apical maxi-K channel density in their CDs (Stoner and Viggiano, J Membr Biol 162: 107116, 1998). The purpose of the present study was to test whether K+ adaptation in the mammalian CCD is associated with upregulation of maxi-K channel expression. New Zealand White rabbits were fed a low (LK), control (CK), or high (HK) K+ diet for 1014 days. Real-time PCR quantitation of message encoding maxi-K
- and
24-subunits in single CCDs from HK animals was greater than that detected in CK and LK animals (P < 0.05);
1-subunit was not detected in any CCD sample but was present in whole kidney. Indirect immunofluorescence microscopy revealed a predominantly intracellular distribution of
-subunits in LK kidneys. In contrast, robust apical labeling was detected primarily in
-intercalated cells in HK kidneys. In summary, K+ adaptation is associated with an increase in steady-state abundance of maxi-K channel subunit-specific mRNAs and immunodetectable apical
-subunit, the latter observation consistent with redistribution from an intracellular pool to the plasma membrane.
potassium adaptation; intercalated cell; principal cell; in vitro microperfusion; H+-K+-ATPase
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