STUDY ON MECHANISM OF ACID AND AMMONIA EXCRETION BY KIDNEY AFTER ACID LOAD

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Abstract
After isotonic hydrochloric acid was infused intravenously into 30 normal, 10 adrenalectomized, and 5 DOCA administered adrenalectomized dogs, changes of acid-base balance in the blood and urine were observed and urinary acidification, as well as ammonia secretion, were investigated. Urinary output of titratable acidity and ammonia increased after the acid infusion and bore an inverse correlation with the blood pH. The reaction was less remarkable in adrenalectomized dogs, while it was restored after the administration of DOCA. 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 DOCA administered dogs. It follows that the mineralcorticoid from the adrenal glands can play an important 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, even though the urinary acidification can be initiated by factors other than the mineralcorticoid. Urinary ammonia clearly bears an inverse correlation with urinary pH; and an appreciable depression in urinary output of ammonia appeared in adrenalectomized dogs. This fact can be explained as due to the decrease of Na+ -NH4 + exchange in the adrenalectomized dog. Concerning renal glutaminase and carbonic anhydrase activity, no difference could be found between normal and adrenalectomized dogs, suggesting no difference in the ability to produce acid and ammonia within renal tubular cells in the two kinds of animals. It follows that a disturbance of the Na+ - H+ and Na+ - NH4 + ion exchange mechanism in the renal tubule of adrenalectomized dogs would result in failure of adaptive increases in the urinary output of acid and ammonia during acute acidosis.

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