Acidosis activation of the pituitary-adrenal-renal glutaminase I axis.
Previous studies have demonstrated that the adrenal glands were necessary for acidosis activation of the mitochondrial glutaminase I pathway. The present studies were undertaken to determine if corticosterone levels are elevated in acidotic rats and if so, whether acidosis stimulates the adrenal glands directly or via the pituitary-adrenal axis. Metabolic acidosis induced by NH4Cl, either acute or chronic, increased corticosterone levels 100 to 130% in intact rats. Acute metabolic acidosis did not activate the mitochondrial pathway in adrenalectomized rats; corticosterone levels were not elevated in hypophysectomized rats nor did activation of the mitochondrial pathway occur in response to acidosis. Therefore, acidosis does not stimulate the adrenal gland directly; rather, it requires the intact pituitary. Administering exogenous corticotropin to hypophysectomized rats resulted in elevation of plasma corticosterone levels and activation of the mitochondrial pathway. The pituitary-adrenal cortex-renal glutaminase I axis apparently operates as a functional unit in the homeostatic response to metabolic acidosis.
D000138:Acidosis / Q000097:blood / Q000378:metabolism*; D000311:Adrenal Glands / Q000502:physiology*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000641:Ammonia / Q000096:biosynthesis; D000818:Animals; D003345:Corticosterone / Q000097:blood*; D005972:Glutaminase / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000201:enzymology; D010902:Pituitary Gland / Q000502:physiology*; D051381:Rats
D000641:Ammonia; D000324:Adrenocorticotropic Hormone; D005972:Glutaminase; D003345:Corticosterone