help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Shibasaki, T.
Right arrow Articles by Ling, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shibasaki, T.
Right arrow Articles by Ling, N.

Journal of Clinical Endocrinology & Metabolism, Vol 56, 414-416, Copyright © 1983 by Endocrine Society

ARTICLES

Pituitary adenomas that caused Cushing's disease or Nelson's syndrome are not responsive to ovine corticotropin-releasing factor in vitro

T Shibasaki, M Nakahara, K Shizume, Y Kiyosawa, T Suda, H Demura, A Kuwayama, N Kageyama, R Benoit and N Ling

The response of pituitary adenomas obtained surgically from patients with Cushing's disease of Nelson's syndrome to synthetic ovine corticotropin-releasing factor (CRF), vasopressins, somatostatin-28, dexamethasone, 3-isobutylmethylxanthine or high [K+] was examined in vitro by measuring the amount of pro-opiomelanocortin (POMC)-derived peptides secreted into the culture medium. CRF did not stimulate the secretion of adrenocorticotropin-, beta-endorphin-, or gamma 3- melanotropin-like peptides from the pituitary adenomas at concentrations ranging from 1 x 10(-13) M to 1 x 10(-7) M whereas vasopressins, 3-isobutyrl-methylxanthine and high [K+] increased, while somatostatin-28 and dexamethasone suppressed, the secretion of these POMC-derived peptides. These findings suggest that either the pituitary ACTH-producing tumors have lost their receptors to CRF or their post- receptor mechanism to CRF is not functional.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. van der Hoek, M. Waaijers, P. M. van Koetsveld, D. Sprij-Mooij, R. A. Feelders, H. A. Schmid, P. Schoeffter, D. Hoyer, D. Cervia, J. E. Taylor, et al.
Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells
Am J Physiol Endocrinol Metab, August 1, 2005; 289(2): E278 - E287.
[Abstract] [Full Text] [PDF]

Home page
 Eur J EndocrinolHome page
L. J Hofland, J. van der Hoek, R. Feelders, M. O van Aken, P. M van Koetsveld, M. Waaijers, D. Sprij-Mooij, C. Bruns, G. Weckbecker, W. W de Herder, et al.
The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5
Eur. J. Endocrinol., April 1, 2005; 152(4): 645 - 654.
[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 © 1983 by The Endocrine Society