K depletion stimulates in vivo hco reabsorption in surviving rat
distal tubules.
Levine, David Z., Michelle Iacovitti, Susan Buckman, Brian Luck,
Maxwell T. Hincke, Kevin D. Burns, and James N. Fryer.
Departments of Medicine and Cellular & Molecular Medicine,
University of Ottawa and Ottawa General Hospital, Ottawa, Ontario,
Canada K1H 8M5
APStracts 5:0002F, 1998.
To evaluate whether K depletion enhances in vivo bicarbonate
reabsorption (JtCO2) in surviving distal tubules (DT), we compared DT
JtCO2 in 5/6 nephrectomized rats (Nx) with and without dietary K
depletion (Nx[angstrom]aK). Further, to identify possible mechanisms
of increased JtCO2, we perfused inhibitors of proton secretion in
both Nx and Nx-K rats. JtCO2 (102[angstrom]a8 pmol[beta]min
-1[beta]mm-1 ) was significantly increased in Nx-K vs Nx rats
(65[angstrom]a7 pmol[beta]min-1[beta]mm-1, P<0.05), but unaffected
by 10-6 M losartan perfusion (94[angstrom]a6 pmol[beta]min-1[beta]mm
-1, P=NS). While 10-5 M Sch-28080 also had no significant effect,
5x10-9 M concanamycin A perfusion significantly decreased JtCO2 in
Nx[angstrom]aK rats to 65[angstrom]a8 pmol[beta] min-1[beta]mm-1,
P<0.05. Morphometric evaluation and H+-ATPase immunogold labelling
of Nx-K A-type intercalated cells revealed cellular hypertrophy,
elaborated apical microplicae, and enhanced H+-ATPase apical
polarization. Accordingly, these combined studies confirm that K
depletion enhances JtCO2 in surviving DT by stimulating H+-ATPase
activity, independent of the AT1 receptor.
Received 17 June 1997; accepted in final form 19 December 1997.
APS Manuscript Number F197-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 January 1998