Although adrenalectomy is usually associated with an impairment of ammonium and/or titratable acid excretion by the kidney, it is uncertain whether rates of renal net acid excretion are also reduced. Further, it is unclear whether the absence of the adrenal gland itself or other factors of adrenal insufficiency mediate such changes in renal acidification parameters. For example, dramatic increases in ammonium excretion can accompany correction of the hyperkalemia seen in adrenal insufficiency. There is also evidence that reduced rates of acid excretion can result from changes in food intake, urine flow rate, urine pH or distal sodium delivery rates. With these considerations in mind, we undertook studies to isolate the chronic effects of adrenalectomy on renal net acid excretion rates in the unanaesthetized rat. To avoid supranormal potassium stores, we gave the adrenalectomized animals potassium-restricted diets. In balance studies, urine flow rates, urine pH, food intake, and distal sodium delivery rates were all successfully controlled for 13 days by pair feeding and by appropriately changing the sodium and potassium contents of diets. Adrenalectomized rats excreted less net acid than did control animals with or without ammonium chloride loading. Further, the severe metabolic acidosis associated with ammonium chloride loading was clearly mitigated by steroid replacement. Accordingly, we conclude that the adrenal gland is essential for normal renal net acid excretion.
Acid-Base Equilibrium Acidosis