Effect of luminal angiotensin ii on ammonia production and secretion by mouse proximal tubules. Nagami, Glenn T., With The Technical Assistance Of Evelyn M. Warech. Departments: Medical and Research Services, Department of Veterans Affairs Medical Center, West Los Angeles, Los Angeles, CA 90073, and Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA 90024
APStracts 2:0014F, 1995.
Angiotensin II is an important regulator of acid-base and ammonia metabolism in the proximal tubule. Because angiotensin II receptors exist on the apical membrane and because luminal fluid angiotensin II concentrations may be substantial, the effects of luminal angiotensin II on ammonia production rates and net luminal tNH3 secretion rates were examined in dissected mouse S2 proximal tubule segments. Ammonia production rates reflected the total release of ammonia via the basolateral and luminal aspects of the tubule while net luminal secretion rates reflected the rates at which ammonia left the tubule via the luminal fluid leaving the distal end of the perfused segment. The results demonstrated that: 1) luminal angiotensin II affected tNH3 production in a concentration-dependent fashion; 2) luminal angiotensin II at concentrations which stimulated tNH3 production could counteract the effect of inhibitory basolateral concentrations of angiotensin II; 3) both the stimulation of tNH3 production and the rise in intracellular calcium concentration induced by 10-10 M luminal angiotensin II were blocked by the addition of an angiotensin II receptor inhibitor, saralasin, or the calcium channel blocker, nifedipine, to the luminal perfusion solution; and 4) in contrast to basolateral angiotensin II which inhibited net luminal tNH3 secretion, luminal angiotensin II stimulated amiloride-sensitive net luminal tNH3 secretion in parallel with stimulation of luminal fluid acidification. Thus, luminal angiotensin II at physiologic and superphysiologic concentrations has important effects on ammonia production and transport in the proximal tubule which in some ways differ from the effects of basolateral angiotensin II. 

Received 8 December 1994; accepted in final form 6 February 1995.
APS Manuscript Number F436-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 February 1995.