JOE
HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Endocrinology (2007) 192, 453-458       DOI: 10.1677/JOE-06-0103
© 2007 Society for Endocrinology
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Raff, H.
Right arrow Articles by Jacobson, L.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Raff, H.
Right arrow Articles by Jacobson, L.

Glucocorticoid feedback control of corticotropin in the hypoxic neonatal rat

Hershel Raff and Lauren Jacobson1

Endocrine Research Laboratory, Aurora St Luke’s Medical Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53215, USA
1 Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA

(Requests for offprints should be addressed to H Raff who is now at Endocrinology, St Luke’s Physician’s Office Building, 2801 W. KK River Pky, Suite 245, Milwaukee, Wisconsin 53215, USA; Email: hraff{at}mcw.edu)

The objective of this study was to determine the effects of manipulating glucocorticoid negative feedback on acute ACTH and corticosterone responses to corticotropin-releasing hormone (CRH) injection in 7-day-old rats exposed to normoxia or hypoxia from birth. Chemical adrenalectomy was achieved with aminoglutethimide, and glucocorticoids were replaced with a low dose of dexamethasone. Hypoxia per se increased basal plasma corticosterone and attenuated the plasma ACTH response to CRH. Aminoglutethimide per se decreased plasma corticosterone and strongly increased basal plasma ACTH and anterior pituitary POMC gene expression. Dexamethasone partially attenuated elevations in basal plasma ACTH due to aminoglutethimide in both normoxic and hypoxic pups, but inhibited anterior pituitary POMC expression and CRH-induced plasma ACTH only in hypoxic pups. Despite this inhibition, hypoxic pups treated with both dexamethasone and aminoglutethimide still exhibited a significant CRH-induced increment in plasma ACTH, which was lacking in hypoxic pups not treated with either dexamethasone or aminoglutethimide. We conclude that ACTH responses to acute stimuli in hypoxic neonatal rats are prevented by ACTH-independent increases in corticosterone, rather than by intrinsic hypothalamic–pituitary hypoactivity.




This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
E. D. Bruder, J. K. Taylor, K. J. Kamer, and H. Raff
Development of the ACTH and corticosterone response to acute hypoxia in the neonatal rat
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1195 - R1203.
[Abstract] [Full Text] [PDF]




HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the Society for Endocrinology.