Riondel A M, Rebuffat P, Mazzochi G, Nussdorfer G G, Gaillard R C, Bockhorn L, Nussberger J, Vallotton M B, Muller A F
Acta Endocrinol (Copenh). 1987 Jan;114(1):47-54. doi: 10.1530/acta.0.1140047.
To test the hypothesis that the trophic action of angiotensin II on the adrenal zona glomerulosa may allow a sustained stimulation of aldosterone by ACTH by preventing the morphological changes of the zona glomerulosa cells into zona fasciculata-like elements we investigated the effects in rats of a 6-day treatment with ACTH (100 micrograms/kg/day) alone or combined with angiotensin II (300 ng/kg/day) on corticosterone and aldosterone production and adrenal morphology. The responsiveness of both steroids to an acute ACTH dose was also studied on the last day of long-term treatment. Morphologic data showed that prolonged ACTH treatment stimulated the growth of zona glomerulosa cells, though it transformed the tubulo-lamellar cristae of mitochondria into a homogeneous population of vesicles. Angiotensin II furthered the trophic effects of ACTH but prevented the mitochondrial transformation. Despite its ability to conserve the well differentiated aspect of the zona glomerulosa cells, the administration of angiotensin II was unable to prevent the fall in the secretion of aldosterone caused by chronic ACTH treatment and its subsequent unresponsiveness to ACTH stimulation.
血管紧张素II对肾上腺球状带的营养作用可通过防止球状带细胞转变为束状带样细胞形态变化，从而使促肾上腺皮质激素（ACTH）持续刺激醛固酮分泌，我们研究了单独给予ACTH（100微克/千克/天）或联合血管紧张素II（300纳克/千克/天）对大鼠进行6天治疗后，对皮质酮和醛固酮生成以及肾上腺形态的影响。在长期治疗的最后一天，还研究了两种类固醇对急性ACTH剂量的反应性。形态学数据显示，长期ACTH治疗刺激了球状带细胞的生长，尽管它将线粒体的管状板层嵴转变为均匀的囊泡群体。血管紧张素II进一步增强了ACTH的营养作用，但阻止了线粒体的转变。尽管血管紧张素II能够保持球状带细胞良好的分化状态，但它无法阻止慢性ACTH治疗引起的醛固酮分泌下降及其随后对ACTH刺激的无反应性。
