Regulation of luminal alkalinization and acidification in the
cortical collecting duct by angiotensin ii.
Weiner, I. David, Andrea R. New, Amy E. Milton, and C. Craig Tisher.
Division of Nephrology, Hypertension and Transplantation,
University of Florida, Gainesville, FL 32610 and Gainesville VA
Medical Center, Gainesville, FL 32608
APStracts 2:0096F, 1995.
Angiotensin II (AII) regulates whole kidney ion transport, yet its
effects in the collecting duct are unknown. The purpose of these
studies was to determine whether AII regulates luminal alkalinization
and acidification in the rabbit cortical collecting duct (CCD). The
rate of luminal alkalinization or acidification was measured as the
rate of change of luminal fluid pH under stop-flow conditions using
in vitro microperfused CCD segments. Outer CCD alkalinized the
luminal fluid, consistent with net HCO3 secretion. Addition of AII,
10-7M, to the peritubular solution for 30 minutes significantly
stimulated luminal alkalinization. The stimulatory effect of AII was
not due to time-dependent effects and was blocked by peritubular
addition of the angiotensin II type 1 (AT1) receptor antagonist,
Losartan, 10-6M. Losartan, 10-6M, when added to the peritubular
solution did not alter the rate of luminal alkalinization independent
of AII. In contrast, peritubular AII, 10-7M, did not alter inner CCD
luminal acidification. Addition of AII to the peritubular solution at
the lower concentration of 10-10M did not alter the rates of luminal
alkalinization and acidification in the outer and inner CCD,
respectively. Peritubular AII, 10 7M, but not vehicle, stimulated B
cell apical HCO3 secretion occurring in response to peritubular Cl
removal. These studies demonstrate that AII acts through a
basolateral AT1 receptor to stimulate outer CCD luminal
alkalinization via, at least in part, B cell stimulation.
Received 12 July 1994; accepted in final form 23 May 1995.
APS Manuscript Number F241-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.