Regulation of b-type intercalated cell apical anion exchange
activity by co2/hco3.
Milton, Amy E., and I. David Weiner.
Division of Nephrology, Hypertension and Transplantation,
University of Florida College of Medicine, Gainesville, FL 32610, and
Gainesville Veterans' Administration Medical Center, Gainesville, FL
32609
APStracts 5:0050F, 1998.
The cortical collecting duct (CCD) B cell possesses an apical anion
exchanger dissimilar to AE1, AE2 and AE3. The purpose of these
studies was to characterize this transporter more fully by examining
its regulation by CO2 and HCO3-. We measured intracellular pH (pHi)
in single intercalated cells of in vitro microperfused CCD using the
fluorescent, pH-sensitive dye, BCECF. In the absence of extracellular
CO2-HCO3- luminal Cl- removal caused reversible intracellular
alkalinization, identifying this transporter as a Cl-/base exchanger
able to transport bases other than HCO3-. Adding extracellular CO2
-HCO3- decreased B cell pHi while simultaneously increasing Cl-/base
exchange activity. Since intracellular acidification inhibits AE1,
AE2 and AE3, we examined mechanisms other than pHi by which the
stimulation occurred. These studies showed that B cell apical anion
exchange activity was CO2-stimulated and carbonic anhydrase
-dependent. Moreover, the stimulation was independent of luminal
bicarbonate, luminal or intracellular pH and changes in buffer
capacity. We conclude that the B cell possesses an apical Cl--base
exchanger whose activity is regulated by CO2-stimulated, carbonic
anhydrase-dependent cytoplasmic HCO3- formation.
Received 27 August 1997; accepted in final form 19 February 1998.
APS Manuscript Number F277-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 March 1998