Welbourne T C
Endocrinology. 1976 Oct;99(4):1071-9. doi: 10.1210/endo-99-4-1071.
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.
先前的研究表明，肾上腺对于酸中毒激活线粒体谷氨酰胺酶I途径是必需的。本研究旨在确定酸中毒大鼠的皮质酮水平是否升高，若升高，酸中毒是直接刺激肾上腺，还是通过垂体-肾上腺轴刺激肾上腺。氯化铵诱导的急性或慢性代谢性酸中毒，使完整大鼠的皮质酮水平升高了100%至130%。急性代谢性酸中毒未激活肾上腺切除大鼠的线粒体途径；垂体切除大鼠的皮质酮水平未升高，酸中毒也未引起线粒体途径的激活。因此，酸中毒并非直接刺激肾上腺；相反，它需要完整的垂体。给垂体切除大鼠注射外源性促肾上腺皮质激素会导致血浆皮质酮水平升高和线粒体途径激活。垂体-肾上腺皮质-肾谷氨酰胺酶I轴显然作为一个功能单位，参与对代谢性酸中毒的稳态反应。
