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Department of Physiology (S.B.P., L.C.R., R.D.K.), University of Maryland School of Medicine, Baltimore, Maryland 21201; and Department of Molecular and Integrative Physiology and College of Medicine (O.D.S.), University of Illinois, Urbana, Illinois 61801
Address all correspondence and requests for reprints to Robert D. Koos, Ph.D., University of Maryland Medical School, Department of Physiology, 655 West Baltimore Street, Baltimore, Maryland 21201-1559.
Relaxin’s ability to stimulate uterine growth is well established. The mechanisms by which relaxin exerts this effect, however, remain unclear. In light of previous work demonstrating peptide growth factor activation of estrogen receptors (ERs), the present study was conducted to determine if relaxin similarly stimulates ERs. Twenty-five day-old female Sprague-Dawley rats were bilaterally ovariectomized and treated with estradiol or porcine relaxin alone or in combination with the ER antagonist ICI 182,780. Following treatment with 17ß-estradiol or relaxin alone, the uterine weight/body weight ratio (UtW/BW) increaased significantly over control values (+98% and +77%, respectively, p < 0.0003). Pre-treatment of animals with ICI 182,780 (3 µg/g BW) prior to either estradiol or relaxin treatment completely inhibited the hormone-induced increases in uterine weight (p < 0.0005). ICI 182,780 alone had no significant effect. Histological analysis of uterine cross-sections revealed that the edema present in the endometrium of animals treated with estradiol or relaxin alone was completely absent in the uteri of animals pre-treated with ICI 182,780. These data indicate that relaxin-induced uterine edema and growth is mediated by ERs.
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