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  • Title: The differential regulation of aldosterone output in hamster adrenal by angiotensinII and adrenocorticotropin.
    Author: Lehoux JG, Ducharme L.
    Journal: J Steroid Biochem Mol Biol; 1992 Mar; 41(3-8):809-14. PubMed ID: 1373307.
    Abstract:
    Aldosterone was isolated from hamster adrenal cells and was identified by high performance liquid chromatography and thermospray mass spectroscopy analysis. Basal outputs from adrenal cell suspensions were of the same order of magnitude, 8.4 +/- 1.9 ng and 8.0 +/- 0.7 ng/2 h/50,000 cells, for aldosterone and corticosteroid, respectively. The outputs of aldosterone and corticosteroid increased with K+ concentrations to reach maxima of 3.3- and 1.6-fold at 10 meq/l of K+. AngiotensinII (AII) produced dose-dependent increases in aldosterone and corticosteroid outputs with maxima of 3- and 4-fold, respectively. In contrast, ACTH induced relatively no changes in aldosterone output, whereas dose-dependent increases in corticosteroid output were found. In time study experiments, with 10(-8) M AII, aldosterone and corticosteroid outputs were maximally increased after 1 h (6-fold) and 3 h (1.8-fold), respectively. At 10(-8) M, ACTH had a small stimulatory effect on aldosterone output after 6 h, whereas it provoked a gradual increase in corticosteroid output (up to 7-fold after 8 h of incubation). The effects of AII and ACTH on adrenal cytochrome P-450(11 beta) involved in the last steps of aldosterone formation were evaluated by combined in vivo and in vitro experiments. The P-450(11 beta) mRNA level was increased by a low sodium intake but not by a 24 h ACTH stimulus. These results taken together indicate that ACTH and AII differentially regulate P-450(11 beta). It is postulated that these two regulatory peptides regulate the hamster adrenal steroidogenesis by different P-450 genes.
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