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Endocrinology, Vol 134, 1188-1192, Copyright © 1994 by Endocrine Society
ARTICLES |
BJ Geddes, LJ Parry and AJ Summerlee
Department of Biomedical Sciences, University of Guelph, Ontario, Canada.
Experiments were conducted in anesthetized rats to assess the contribution of the brain angiotensin-II system in the relaxin-induced secretion of vasopressin and oxytocin. Intravenous injection of porcine relaxin (5 micrograms) caused a significant (P < 0.05, by analysis of variance) increase in plasma concentrations of both hormones. Peak concentrations of both vasopressin (75.2 +/- 2.9 pmol/liter) and oxytocin (38.4 +/- 1.2 pmol/liter) were observed 1-2.5 min after relaxin injection. Thereafter, concentrations fell significantly (P < 0.05) but remained elevated for a further 25 minutes. Continuous infusion of a specific angiotensin-II receptor antagonist into the lateral cerebral ventricle did not affect baseline levels of either vasopressin or oxytocin, but did significantly reduce (P < 0.05) the relaxin-induced release of both peptides. A significant (P < 0.05) short term increase in both plasma vasopressin and oxytocin occurred 1 min after injection of 5 micrograms relaxin, iv, in angiotensin-II- antagonized rats, but the concentrations of both neuropeptides were significantly (P < 0.05) lower than those observed in the angiotensin- intact relaxin-treated controls. These data suggest that relaxin may act through the central angiotensin-II system to induce the release of vasopressin and oxytocin.
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