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
Right arrow Citation Map
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 Parry, L. J.
Right arrow Articles by Summerlee, A. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parry, L. J.
Right arrow Articles by Summerlee, A. J.

Endocrinology, Vol 129, 47-52, Copyright © 1991 by Endocrine Society

ARTICLES

Central angiotensin partially mediates the pressor action of relaxin in anesthetized rats

LJ Parry and AJ Summerlee
Ontario Veterinary College, University of Guelph, Canada.

Experiments were conducted to investigate the role of the brain angiotensin system in mediating the pressor effects of porcine relaxin in anesthetized female rats. Continuous intracerebroventricular infusion of a specific angiotensin II receptor antagonist (Sar1-Ala8- angiotensin II) completely negated the pressor response to centrally administered relaxin, but only partially suppressed the increase in blood pressure observed after iv injection of the hormone. These results indicate that the pressor effects of relaxin may be mediated, at least in part, by brain angiotensin. Rats with a compromised central angiotensin system were then treated in combination with a peripheral vasopressin (V1) receptor antagonist. Only after both treatments were the pressor effects of iv relaxin completely negated. These data imply that there is also a significant pressor action of relaxin which is independent of the brain angiotensin system. The most likely alternative is a direct action of relaxin on the neural lobe of the pituitary, to provoke the release of vasopressin.


This article has been cited by other articles:


Home page
 Endocr. Rev.Home page
O. D. Sherwood
Relaxin's Physiological Roles and Other Diverse Actions
Endocr. Rev., April 1, 2004; 25(2): 205 - 234.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
P. Sinnayah, P. Burns, J. D. Wade, R. S. Weisinger, and M. J. McKinley
Water Drinking in Rats Resulting from Intravenous Relaxin and Its Modification by Other Dipsogenic Factors
Endocrinology, November 1, 1999; 140(11): 5082 - 5086.
[Abstract] [Full Text]

Home page
 Physiol. Rev.Home page
J. T. FITZSIMONS
Angiotensin, Thirst, and Sodium Appetite
Physiol Rev, July 1, 1998; 78(3): 583 - 686.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
A. J. S. Summerlee, D. J. Hornsby, and D. G. Ramsey
The Dipsogenic Effects of Rat Relaxin: The Effect of Photoperiod and the Potential Role of Relaxin on Drinking in Pregnancy
Endocrinology, May 1, 1998; 139(5): 2322 - 2328.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
A. J. S. Summerlee, D. G. Ramsey, and R. S. Poterski
Neutralization of Relaxin within the Brain Affects the Timing of Birth in Rats
Endocrinology, February 1, 1998; 139(2): 479 - 484.
[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 © 1991 by The Endocrine Society