Grizzle W E, Dunlap N E
Am J Physiol. 1984 Apr;246(4 Pt 1):E306-10. doi: 10.1152/ajpendo.1984.246.4.E306.
We report that adrenal compensatory hypertrophy occurs in intact and hypophysectomized anesthetized rats as well as in rats in which endogenous ACTH is suppressed by administration of dexamethasone or of dexamethasone plus low-dose ACTH. However, adrenal compensatory hypertrophy is blocked in intact and hypophysectomized animals when aldosterone alone or the combination of aldosterone, dexamethasone, and ACTH is administered using Alzet pumps. These data support previous reports that questioned the validity of the hypothesis that adrenal compensatory hypertrophy is controlled by the glucocorticoid-ACTH negative feedback system. These results require modification of current hypotheses concerning the mechanism of adrenal compensatory hypertrophy to allow for a central nervous system or other effect of aldosterone.
我们报告称,肾上腺代偿性肥大发生在完整的、垂体切除的麻醉大鼠中,以及在内源性促肾上腺皮质激素(ACTH)被地塞米松或地塞米松加低剂量ACTH抑制的大鼠中。然而,当使用Alzet泵单独给予醛固酮或给予醛固酮、地塞米松和ACTH的组合时,完整的和垂体切除的动物中的肾上腺代偿性肥大被阻断。这些数据支持了先前的报告,这些报告对肾上腺代偿性肥大受糖皮质激素-ACTH负反馈系统控制这一假说的有效性提出了质疑。这些结果需要修改当前关于肾上腺代偿性肥大机制的假说,以考虑醛固酮的中枢神经系统或其他作用。