Effects of chronic chloride depletion metabolic alkalosis on proximal tubule transport and renal production of ammonium. Dubose, Thomas D., Jr, and David W. Good. Division of Nephrology, Departments of Medicine, Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas, 77555; and Division of Nephrology, Department of Internal Medicine, University of Texas, Medical School, Houston, Texas, 77030
APStracts 2:0077F, 1995.
The role of renal ammonium excretion in the maintenance of chronic metabolic alkalosis is poorly defined, particularly under conditions in which the alkalosis is associated with secondary potassium depletion. Therefore, free-flow micropuncture experiments were performed to examine the effects of chronic chloride depletion metabolic alkalosis (CDAlk) on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule (PCT) ammonium transport in the rat in vivo. CDAlk was generated by peritoneal dialysis against NaHCO3 and maintained for 6-7 days by dietary Cl - restriction. Pair fed controls were dialyzed against NaCl. Rats with CDAlk had elevated plasma [HCO], hypokalemia, and hypochloremia. HCO excretion was negligible in both control and CDAlk rats. Glomerular filtration rate and urine pH did not differ. CDAlk reduced urinary ammonium excretion by 35% but had no significant effect on whole kidney ammonium production. Net secretion of ammonium by the PCT was decreased by 70% and absolute delivery of ammonium out of the PCT was decreased by 55% in the CDAlk rats. The decrease in PCT ammonium secretion was the combined result of a decrease in net ammonium secretion along the early PCT and an increase in net ammonium absorption along the late PCT. These results demonstrate that in a model of hypokalemic CDAlk in the rat: 1) ammonium excretion is decreased, largely due to a decrease in net ammonium secretion by the PCT, 2) there is no detectable change in renal ammonium production, presumably because the inhibitory influence of alkalemia is offset by the stimulatory influence of hypokalemia, 3) ammonium excretion is regulated in a manner that is appropriate for the acid-base disorder and that serves to minimize the rise in plasma bicarbonate concentration during maintenance of the alkalosis. 

Received 19 September 1994; accepted in final form 11 April 1995.
APS Manuscript Number F335-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 16 May 1995.