Estradiol induces C-type natriuretic peptide gene expression in mouse uterus

• Published in: American journal of physiology. Heart and circulatory physiology 1997-12, Vol.273 (6), p.H2672-H2677
• Main Authors: Acuff, Cory G, Huang, Huaming, Steinhelper, Mark E
• Format: Article
• Language: English
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.1997.273.6.h2672

1  Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284-7756; and 2  Vascular Biology and Hypertension Program, Department of Medicine University of Alabama at Birmingham, Birmingham, Alabama 35294 Previous experiments have demonstrated that C-type natriuretic peptide (CNP) expression in the uterus varies during the estrous cycle with maximal expression at proestrus. The present study was designed to determine whether exogenous steroid hormones regulate uterine CNP expression in ovariectomized mice. Estradiol increased significantly (3-fold) uterine immunoreactive CNP (irCNP) rapidly and dose dependently in ovariectomized mice as measured by radioimmunoassay. Other steroids produced either no significant change (testosterone, 1 mg; 2-methoxyestradiol, 1 µg) or weak induction (estriol, 1 µg) from vehicle controls. Progesterone (1 mg) significantly attenuated the estrogen-stimulated irCNP response by 50% when injected 30 min before estrogen (1 µg) in estrogen-primed ovariectomized mice. Estrogen-stimulated increases in uterine CNP transcripts detected by ribonuclease protection analyses were blocked by actinomycin D (160 µg) or ICI-164,384 (20 µg), a specific nuclear estrogen receptor antagonist. These results indicate that a nuclear estrogen receptor is required for estrogen to stimulate uterine CNP transcription and that progesterone negatively regulates estrogen-stimulated CNP expression. hydromineral homeostasis; reproduction; hyperemia; steroid hormones; estrous cycle