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 Lymangrover, J. R.
Right arrow Articles by Saffran, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lymangrover, J. R.
Right arrow Articles by Saffran, M.

Endocrinology, Vol 110, 462-468, Copyright © 1982 by Endocrine Society

ARTICLES

Membrane potential changes of mouse adrenal zona fasciculata cells in response to adrenocorticotropin and adenosine 3',5'-monophosphate

JR Lymangrover, EK Matthews and M Saffran

ACTH superfused onto mouse adrenal zona fasciculata tissue caused a transient, dose-dependent membrane depolarization. The log of the dose of ACTH was linearly related to the magnitude of depolarization. The onset of depolarization was rapid and dose dependent. Resting membrane potential changes observed after ACTH were blocked by CoCl2 but not tetrodotoxin or 4-aminopyridine, indicating that these depolarizations were dependent primarily on transmembrane Ca++ flux. CoCl2 also significantly blocked ACTH-stimulated adrenal steroid production; 4- aminopyridine had a much smaller and greatly delayed effect, whereas tetrodotoxin had no detectable effect on steroidogenesis. cAMP administration to adrenal zona fasciculata cells elicited transient, dose-dependent membrane depolarizations, which closely resembled those observed after ACTH treatment. In contrast to ACTH, CoCl2 did not block the cAMP-induced depolarization. These and other studies indicate that ACTH initiates a complex series of events by which steroidogenesis is stimulated. One mechanism may involve a change in membrane permeability to Ca++ independently of cAMP generation; a second mechanism may involve the activation of adenylate cyclase which subsequently influences the membrane conductance of the fasciculata cell membrane.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
J. J. Enyeart, S. J. Danthi, H. Liu, and J. A. Enyeart
Angiotensin II Inhibits bTREK-1 K+ Channels in Adrenocortical Cells by Separate Ca2+- and ATP Hydrolysis-dependent Mechanisms
J. Biol. Chem., September 2, 2005; 280(35): 30814 - 30828.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. J. Enyeart, L. Xu, and J. A. Enyeart
Dual actions of lanthanides on ACTH-inhibited leak K+ channels
Am J Physiol Endocrinol Metab, June 1, 2002; 282(6): E1255 - E1266.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J. A. Enyeart, L. Xu, and J. J. Enyeart
A Bovine Adrenocortical Kv1.4 K+ Channel Whose Expression Is Potently Inhibited by ACTH
J. Biol. Chem., October 27, 2000; 275(44): 34640 - 34649.
[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 © 1982 by The Endocrine Society