Cortical collecting duct with chronic metabolic acidosis.
Silver, Randi B., Patricia Mennitt, and Lisa M. Satlin.
Dept. of Physiology, Cornell University Medical College, 1300 York
Avenue, New York, NY 10021 and Dept. of Pediatrics, Albert Einstein
College of Medicine, 1410 Pelham Parkway South, Bronx, N.Y. 10461
APStracts 2:0183F, 1995.
This study evaluated the role of H-K ATPase with chronic metabolic
acidosis (CMA) in intercalated cells (ICs) of rabbit cortical
collecting duct (CCD). CMA was induced by replacing drinking water
with 75 mM NH4Cl in 5 % sucrose for 10-14 days. CCDs isolated from
CMA and control rabbits were split-opened and exposed to the
intracellular pH indicator 2',7'-bis(carboxyethyl)-5(6)
-carboxyfluorescein (BCECF). In Hepes buffered solutions the resting
intracellular pH (pHi) in ICs was similar for both groups. K
-dependent pHi recovery (5 mM K, 140 mM NMDG) was monitored in
response to a pulse of NH4Cl (10 mM). The K-dependent pHi recovery
rate was 3-fold higher in CMA ICs compared to controls and was
abolished with the gastric H-K ATPase inhibitor SCH 28080 (10-5 M).
Polarity of the H-K ATPase was studied in microperfused CMA and
control CCDs. Luminal K-dependent pHi recovery was monitored in
response to an acute pulse of NH4Cl in individual peanut lectin
binding (PNA) ICs. The apical SCH 28080 - inhibitable K-dependent pHi
recovery rate was significantly greater in CMA ICs than control ICs.
In summary CMA enhances functional activity of an apical H-K ATPase
in PNA ICs of rabbit CCD.
Received 9 January 1995; accepted in final form 28 September
1995.
APS Manuscript Number F3-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95