help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cozza, E. N.
Right arrow Articles by Gomez-Sanchez, C. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cozza, E. N.
Right arrow Articles by Gomez-Sanchez, C. E.

Endocrinology, Vol 126, 2169-2176, Copyright © 1990 by Endocrine Society

ARTICLES

Treatment of primary cultures of calf adrenal glomerulosa cells with adrenocorticotropin (ACTH) and phorbol esters: a comparative study of the effects on aldosterone production and ACTH signaling system

EN Cozza, MC Vila, M Acevedo-Duncan, RV Farese and CE Gomez-Sanchez
Department of Internal Medicine and Biochemistry, University of South Florida, Tampa 33612.

We studied the mechanism that underlies the desensitization of calf adrenal glomerulosa cells induced by 4 h of ACTH treatment. In control cells, acute ACTH treatment provoked sizeable increases in aldosterone, cAMP, and diacylglycerol, and translocated protein kinase-C from cytosol to membrane. In desensitized cells, acute ACTH effects on aldosterone and cAMP decreased by 25-60%, and diacylglycerol levels and protein kinase-C translocation were persistently stimulated and not substantially affected by further acute ACTH treatment. After 4 h of treatment with 1 microM phorbol 12-myristate 13-acetate (PMA) there were no acute effects of ACTH on the production of aldosterone, cAMP, or diacylglycerol or on protein kinase-C, which was already strongly translocated. These results suggest that ACTH-mediated desensitization of calf adrenal glomerulosa cells may be at least partially mimicked by long term treatment with phorbol esters and could be due to ACTH- induced increases in diacylglycerol-protein kinase-C signaling.


This article has been cited by other articles:


Home page
 J EndocrinolHome page
P. Ye, B. Mariniello, F. Mantero, H. Shibata, and W. E Rainey
G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism
J. Endocrinol., October 1, 2007; 195(1): 39 - 48.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
Z. Kilianova, N. Basora, P. Kilian, M. D. Payet, and N. Gallo-Payet
Human Melanocortin Receptor 2 Expression and Functionality: Effects of Protein Kinase A and Protein Kinase C on Desensitization and Internalization
Endocrinology, May 1, 2006; 147(5): 2325 - 2337.
[Abstract] [Full Text] [PDF]

Home page
 J EndocrinolHome page
J. M C Connell and E. Davies
The new biology of aldosterone
J. Endocrinol., July 1, 2005; 186(1): 1 - 20.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1990 by The Endocrine Society