title: Upregulation of angiotensin II type 2 receptor expression in estrogen-induced pituitary hyperplasia.
abstract: Recent evidence shows that reexpression and upregulation of angiotensin II (ANG II) type 2 (AT2) receptor in adult tissues occur during pathological conditions such as tissue hyperplasia, inflammation, and remodeling. In particular, expression of functional AT2 receptors in the pituitary and their physiological significance and regulation have not been described. In this study, we demonstrate that chronic in vivo estrogen treatment, which induces pituitary hyperplasia, enhances local AT2 expression (measured by Western blot and RT-PCR) concomitantly with downregulation of ANG II type 1 (AT1) receptors. In vivo progesterone treatment of estrogen-induced pituitary hyperplasia did not modify either the ANG II receptor subtype expression pattern or octapeptide-induced and AT1-mediated calcium signaling. Nevertheless, an unexpected potentiation of the ANG II prolactin-releasing effect was observed in this group, and this response was sensitive to both AT1 and AT2 receptor antagonists. These data are the first to document that ANG II can act at the pituitary level through the AT2 receptor subtype and that estrogens display a differential regulation of AT1 and AT2 receptors at this level.
authors.affiliation: Instituto de Biología y Medicina Experimental-Consejo Nacional de Investigaciones Cieníficas y Técnicas y Técnicas, 1428 Buenos Aires, Argentina.
authors.forename: Cecilia
authors.initials: C
authors.lastname: Suarez
authors.forename: Graciela
authors.initials: G
authors.lastname: Díaz-Torga
authors.forename: Arturo
authors.initials: A
authors.lastname: González-Iglesias
authors.forename: Carolina
authors.initials: C
authors.lastname: Cristina
authors.forename: Damasia
authors.initials: D
authors.lastname: Becu-Villalobos
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D004054:Diethylstilbestrol / Q000008:administration & dosage; D015536:Down-Regulation; D004968:Estrogens, Non-Steroidal / Q000008:administration & dosage; D005260:Female; D006965:Hyperplasia / Q000139:chemically induced; D010900:Pituitary Diseases / Q000139:chemically induced / Q000378:metabolism*; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D011388:Prolactin / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D004968:Estrogens, Non-Steroidal; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D019326:17-alpha-Hydroxyprogesterone; D004054:Diethylstilbestrol; D011388:Prolactin