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This Article Full Text Full Text (PDF) All Versions of this Article: 286/5/E786    most recent 00477.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Suarez, C. Articles by Becu-Villalobos, D. Search for Related Content PubMed PubMed Citation Articles by Suarez, C. Articles by Becu-Villalobos, D.

Upregulation of angiotensin II type 2 receptor expression in estrogen-induced pituitary hyperplasia

Instituto de Biología y Medicina Experimental-Consejo Nacional de Investigaciones Científicas y Técnicas, 1428 Buenos Aires, Argentina

Submitted 21 October 2003 ; accepted in final form 5 January 2004

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.

prolactin; calcium signaling; Western blot; reverse transcriptase-polymerase chain reaction

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