Renal ammonia excretion during acetazolamide or sodium bicarbonate administration

Abstract

Measurements of ammonia and inulin concentration and pH were performed on samples of proximal or distal tubular fluid from 49 diuretic rats treated with either acetazolamide or sodium bicarbonate. The ammonia concentration in midproximal tubular fluid was not altered by acetazolamide despite an apparent elevation of tubular fluid pH to 7.23[plus or minus].09 units (quin-hydrone electrode). During acetazolamide administration, proximal ammonia was sufficient to account for 150% of urinary ammonia and 300% of the ammonia in distal tubular fluid. During an infusion of sodium bicarbonate, the ammonia concentration fell to < 0.3 mM in midproximal tubular fluid despite an elevation of apparent tubular fluid pH (quinhydrone electrode) which was similar to that observed during acetazolamide administration. Estimates of the PNH3 in proximal and distal fluid suggest that diffusion equilibrium for ammonia does exist between blood and cortical tubular fluids. The results further emphasize the quantitative importance of the proximal fluid ammonia as a potential source of urine ammonia, and they clearly demonstrate that the large amounts of ammonia which are added to proximal fluid may be subsequently reabsorbed at some point between the midproximal and early distal tubule[long dash]presumably within the loop of Henle.