A Study of the Mechanisms by Which Adrenocorticotropic Hormone Maintains Adrenal Steroidogenic Responsiveness

Robert L. Ney; Richard N. Dexter; Warren W. Davis; Leonard D. Garren

doi:10.1172/JCI105681

^{Department of Medicine, Vanderbilt University, Nashville, Tennessee, the National Heart Institute, Bethesda, Maryland}

^{Department of Internal Medicine, Yale University, New Haven, Connecticut}

Received for publication 26 May 1967 and in revised form 21 July 1967.

Presented in part at the national meeting of the American Federation for Clinical Research, 1 May 1966.

Supported by U. S. Public Health Service Grants 1RO1 AM 10134, 1 RO1 AM 10947, 9070-41-48818, and T1-AM-5092.

Address requests for reprints to Dr. Robert L. Ney, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, N. C. 27514.

Find articles by Ney, R. in: JCI | PubMed | Google Scholar

^{Department of Medicine, Vanderbilt University, Nashville, Tennessee, the National Heart Institute, Bethesda, Maryland}

^{Department of Internal Medicine, Yale University, New Haven, Connecticut}

Received for publication 26 May 1967 and in revised form 21 July 1967.

Presented in part at the national meeting of the American Federation for Clinical Research, 1 May 1966.

Supported by U. S. Public Health Service Grants 1RO1 AM 10134, 1 RO1 AM 10947, 9070-41-48818, and T1-AM-5092.

Address requests for reprints to Dr. Robert L. Ney, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, N. C. 27514.

Find articles by Dexter, R. in: JCI | PubMed | Google Scholar

^{Department of Medicine, Vanderbilt University, Nashville, Tennessee, the National Heart Institute, Bethesda, Maryland}

^{Department of Internal Medicine, Yale University, New Haven, Connecticut}

Received for publication 26 May 1967 and in revised form 21 July 1967.

Presented in part at the national meeting of the American Federation for Clinical Research, 1 May 1966.

Supported by U. S. Public Health Service Grants 1RO1 AM 10134, 1 RO1 AM 10947, 9070-41-48818, and T1-AM-5092.

Address requests for reprints to Dr. Robert L. Ney, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, N. C. 27514.

Find articles by Davis, W. in: JCI | PubMed | Google Scholar

^{Department of Medicine, Vanderbilt University, Nashville, Tennessee, the National Heart Institute, Bethesda, Maryland}

^{Department of Internal Medicine, Yale University, New Haven, Connecticut}

Received for publication 26 May 1967 and in revised form 21 July 1967.

Presented in part at the national meeting of the American Federation for Clinical Research, 1 May 1966.

Supported by U. S. Public Health Service Grants 1RO1 AM 10134, 1 RO1 AM 10947, 9070-41-48818, and T1-AM-5092.

Address requests for reprints to Dr. Robert L. Ney, Department of Medicine, School of Medicine, University of North Carolina, Chapel Hill, N. C. 27514.

Find articles by Garren, L. in: JCI | PubMed | Google Scholar

Published in Volume 46, Issue 12 on December 1, 1967
J Clin Invest. 1967;46(12):1916–1924. https://doi.org/10.1172/JCI105681.
© 1967 The American Society for Clinical Investigation

Published December 1, 1967 - Version history

Following hypophysectomy in the rat, there was a progressive decline in the rate of adrenal protein synthesis in vivo during the ensuing 24-48 hr, and an accompanying decrease in the acute corticosterone secretory response to an intravenous injection of ACTH. There was a similar decrease in the in vitro conversion of Δ⁵-pregnenolone, progesterone, and deoxycorticosterone to corticosterone. These in vivo and in vitro effects of hypophysectomy could be reversed by the administration of depot ACTH for an additional 7 hr period. However, if cycloheximide, an inhibitor of protein synthesis, was administered concomitantly with the depot ACTH, then the restorative actions of ACTH on the steroid biosynthetic pathway were prevented. These experiments suggest that ACTH maintains not only the general structure of the adrenal cortex, but also the level of the steroid biosynthetic mechanism, through its effects on adrenal protein synthesis.