The role of glucocorticoids in external glutamine mobilization and renal utilization was evaluated in three groups of chronically acidotic rats: sham-treated controls, adrenalectomized, and adrenalectomized supplemented with triamcinolone. Chronic acidosis was induced by administering NH4Cl in their drinking solution over a three-day period. Adrenalectomized rats were supplemented by triamcinolone at a dose of 40 micrograms/100 g/d administered by pellet implantation. Interorgan glutamine flow was evaluated in the postabsorptive state by monitoring net balances across the hindquarters, gut, liver, and kidneys. In the adrenal-intact group, acidosis increased the flow of glutamine from the hindquarters to the kidneys; splanchnic bed uptake, the major glutamine sink in nonacidosis, was eliminated by virtue of hepatic reversal from net uptake to release. Adrenalectomy, in the absence of an exogenous acid load, reversed the flow of glutamine with the kidneys releasing and the hindquarters removing glutamine. Acid loading restored hindquarter glutamine release to levels seen in the intact chronically acidotic animals; however, renal extraction is much less than that exhibited by the intact animals. As a consequence, arterial glutamine concentration rose with the overflow removed by the splanchnic bed, the major glutamine sink in adrenalectomized acidotic rats. Supplementing adrenalectomized acidotic rats with triamcinolone restored glutamine extraction to values seen in intact acidotic rats. Despite the renal extraction, the large hindquarter glutamine release led to hepatic uptake and a high rate of ureagenesis. Glucocorticoids, the release of which is enhanced in metabolic acidosis, appear essential for renal glutamine extraction while playing a lesser role in modulating hindquarter glutamine release.(ABSTRACT TRUNCATED AT 250 WORDS)