Study on mechanism of acid and ammonia excretion by kidney after acid load.

Abstract

After isotonic hydrochloric acid was infused intravenously into 30 normal, 10 adrenalectomized and 5 DCA administered adrenalectomized dogs, changes of acid-base balance in the blood and urine were observed and the urinary acidification as well as of ammonia secretion was investigated.The results obtained are summarized as follows:1. Urinary output of titratable acidity and ammonia increased after the acid infusion and bore an inverse correlation with the blood pH. Acid urine formation was less remarkable in adrenalectomized dogs, while it was restored after the administration of DCA.2. A positive correlation was found between plasma potassium concentration and urinary titratable acidity. The amount of titratable acidity is, however, lower in adrenalectomized dogs than normal dogs at the same plasma potassium concentration, while it is higher in DCA administered dogs.3. It follows that the mineralcorticoid from the adrenal glands can play an importantant role in acid urine formation, probably by promoting an ion exchange mechanism of H+ for Na+ across the cell membrane of the renal tubule in acidosis. The fact that the acid urine can also be produced even in the adrenalectomized dog, though to a lesser extent, indicates that the urinary acidification can be initiated by the other factor than the mineralcorticoid. The direct effect of acidosis was suggested as the other factor, which may influence the H+ ion secretion mechanism of tubular cell in association with either K+ deficiency or pH decrease in the cells.4. Urinary ammonia bears a clear inverse correlation with urinary pH, and an appreciable depression in urinary output of ammonia appeared in adrenalectomized dog, and this fact can be explained as due to the decrease of Na+-NH4+ exchange in adrenalectomized dog. The predominance of the ion exchange theory over the capture-by-diffusion theory in mammals for the urinary ammonia excretion was discussed.5. About the renal glutaminase and carbonic anhydrase activity, no difference could be found between normal and adrenalectomized dogs, suggesting no difference in the ability of production of acid and ammonia within the renal tubular cell in two kinds of animals.6. It follows that a disturbance of Na+-H+ and Na+-NH4+ ion exchange mechanism in the renal tubule in adrenalectomized dogs would result in a failure of adaptive increase of urinary output of acid and ammonia in acute acidosis.7. It is confirmed with dog experiments that the increase of urinary ammonia in prolonged acidosis is due to an adaptive increase of renal glutaminase.