Intact ability to lower urine pH in nonacidotic adrenalectomized rats

Distal acidification was assessed in adrenalectomized (ADX) rats in which the development of acidosis was prevented by oral supplementation with NaHCO3, with or without glucocorticoid replacement. Totally corticosteroid-deficient nonacidotic rats were capable of lowering their urine pH in response to Na2SO4 infusion from a baseline of 7.47 +/- 0.22 to 4.83 +/- 0.1 (p less than 0.001). A similarly intact ability to lower the urine pH was also demonstrated in glucocorticoid-replaced mineralocorticoid-deficient rats. Absolute ammonium excretion was lower in ADX animals compared to controls (0.79 +/- 0.08 vs. 0.46 +/- 0.06 microEq/min, p less than 0.01) but when corrected for the difference in GFR, ammonium excretion was the same in ADX and adrenal-intact rats. During bicarbonate loading and at similar blood and urine pH, and bicarbonate concentrations, the U-B pCO2 gradient was similar in mineralocorticoid-deficient and adrenal intact rats (44 +/- 5.1 vs. 36 +/- 2.6 mm Hg, respectively). Amiloride administration to mineralocorticoid-deficient rats led to a reduction in the U-B pCO2 gradient from 30 +/- 4.5 to 10 +/- 3.0 mm Hg (p less than 0.002). These results indicate that the ability to lower the urine pH and raise the urine pCO2 is intact in the nonacidotic ADX rat; ammonium excretion in this model is reduced in proportion to the observed reduction in GFR, and amiloride administration inhibits acidification in ADX rats. The data strongly suggest the presence of a major site of aldosterone-independent, sodium-dependent acidification mechanism likely located at the level of the cortical collecting tubule.