help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
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 Iwasaki, Y.
Right arrow Articles by Robertson, G. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Iwasaki, Y.
Right arrow Articles by Robertson, G. L.

Endocrinology, Vol 134, 48-54, Copyright © 1994 by Endocrine Society


ARTICLES

The effect of the nonselective opioid antagonist diprenorphine on vasopressin secretion in the rat

Y Iwasaki, MB Gaskill, CA Boss and GL Robertson
Department of Medicine, University of Chicago, Illinois 60637.

Although endogenous opioids are thought to be involved in the regulation of vasopressin secretion, their precise role is unclear. We studied the effect of the potent nonselective opioid antagonist diprenorphine on the vasopressin response to osmotic (hypertonic saline, ip), hypovolemic (polyethylene glycol, ip), and hypotensive (sodium nitroprusside, sc) stimuli in male rats. We found that diprenorphine sc produced a time- and dose-dependent inhibition of the plasma vasopressin response to the hypovolemic stimulus. This inhibition was greatest 30 min after injection of the drug, but lasted for at least 4 h, was evident at doses as low as 0.0022 mumol/kg, and reached a maximum of about 85% of the stimulated control at a dose of 2.2 mumol/kg. Diprenorphine also inhibited the vasopressin response to an osmotic or a hypotensive stimulus, but the effect was less complete (approximately 50%), required 100-fold higher doses of the drug, and appeared to be bimodal. The potent kappa 1-selective opioid agonist U- 50,488H also suppressed the vasopressin response to these stimuli, but the effect was not selective for hypovolemia, and the doses required (0.135-13.5 mumol/kg) were about 10- to 100-fold higher than those of diprenorphine. We postulate, therefore, that diprenorphine potently and preferentially inhibits the vasopressin response to an acute hypovolemic stimulus by antagonizing the effect of some endogenous opioidergic system critical in the volume control system.


This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
S. Kakiya, H. Arima, H. Yokoi, T. Murase, Y. Yambe, and Y. Oiso
Effects of acute hypotensive stimuli on arginine vasopressin gene transcription in the rat hypothalamus
Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E886 - E892.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
H. Arima, K. Kondo, T. Murase, H. Yokoi, Y. Iwasaki, H. Saito, and Y. Oiso
Regulation of Vasopressin Synthesis and Release by Area Postrema in Rats
Endocrinology, April 1, 1998; 139(4): 1481 - 1486.
[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 © 1994 by The Endocrine Society