THE RENAL REGULATION OF ACID-BASE BALANCE IN MAN. IV. THE NATURE OF THE RENAL COMPENSATIONS IN AMMONIUM CHLORIDE ACIDOSIS 1

Abstract

Ammonium chloride was given in divided dosage to 2 healthy adult subjects in order (a) to relate the rates of excretion of the several ions to their respective plasma concns; (b) to determine the nature and extent of the changes in glo-merular filtration, renal plasma flow, and ionic reabsorption which underlie altered excretory functions in metabolic acidosis; and (c) to study the time relations of the renal compensations to acidosis. Following the ingestion of NH4 Cl, plasma bicarbonate fell in exact proportion to the increase in plasma chloride, so that the sum of these anions remained unchanged. During the recovery phase, plasma bicarbonate rose more rapidly than chloride fell, resulting in an increase in the sum of these anions. Early in acidosis the excess urinary chloride was neutralized for the most part by Na derived from body buffers. Three different mechanisms were responsible for the restriction of Na loss and the restoration of body buffer reserves: (a) following the ingestion of an acidifying salt, the increase in chloride reabsorption per 100 ml. of glomerular filtrate significantly diminished the loss of fixed base; (b) the increased excretion of K and Ca on the 2d and 3d days of acidosis permitted a decrease in Na excretion although total fixed base loss increased; (c) ammonia and titratable acid production increased progressively during acidosis permitting the continued excretion of acid with a reduction in the loss of fixed base.