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Research Article Free access | 10.1172/JCI107247
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Find articles by Peytremann, A. in: JCI | PubMed | Google Scholar
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Find articles by Nicholson, W. in: JCI | PubMed | Google Scholar
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Find articles by Brown, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Find articles by Liddle, G. in: JCI | PubMed | Google Scholar
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Department of Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
Find articles by Hardman, J. in: JCI | PubMed | Google Scholar
Published April 1, 1973 - More info
The comparative effects of angiotensin II and adrenocorticotropic hormone (ACTH) on cyclic AMP and steroidogenesis were investigated employing isolated bovine adrenal cells from the zona fasciculata. Like ACTH, angiotensin produced a prompt increase in cyclic AMP which preceded the increase in corticosteroid production. Although this increase in cyclic AMP was small when compared to that induced by ACTH, it correlated with the amount of steroidogenesis. This observation is consistent with the view that cyclic AMP is the intracellular mediator of the steroidogenic action of angiotensin.
Angiotensin acted synergistically with ACTH on cyclic AMP levels. This synergism was not explained by inhibition of phosphodiesterase activity. Unlike ACTH, angiotensin failed to stimulate adenylate cyclase in broken cell preparations. The observations suggest that more than one mechanism may be involved in effects of ACTH and angiotensin on cyclic AMP levels.