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This Article Full Text Full Text (PDF) All Versions of this Article: 565/1/85    most recent jphysiol.2005.085753v2 jphysiol.2005.085753v1 Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Byers, M. J. Articles by Magness, R. R. Search for Related Content PubMed PubMed Citation Articles by Byers, M. J. Articles by Magness, R. R.

¹ Perinatal Research Laboratories
² Department of Pediatrics and Animal Sciences, Department of Obstetrics and Gynecology, University of Wisconsin–Madison, Atrium-B Meriter Hospital/Park, Madison, WI 53715, USA

Pregnancy and the follicular phase are physiological states of elevated oestrogen levels and rises in uterine blood flow (UBF). The dramatic increase in utero-placental blood flow during gestation is required for normal fetal growth and development. Oestrogen exerts its vasodilatory effect by binding to its specific oestrogen receptors (ER) in target cells, resulting in increased expression and activity of endothelial nitric oxide synthase (eNOS) to relax vascular smooth muscle (VSM). However, the regulation of endothelial versus VSM ER and ERß expression in uterine arteries (UAs) during the ovarian cycle, pregnancy and with exogenous hormone replacement therapy (HRT) are currently unknown. ER mRNA and protein localization was determined by in situ hybridization (ISH) using ³⁵S-labelled riboprobes and immunohistochemistry (IHC), respectively. UA endothelial (UAendo), UA VSM, omental artery endothelium (OA endo), and OA VSM proteins were isolated and ER and ERß protein expression was determined by Western analysis. We observed by ISH and IHC that ER and ERß mRNA and protein were localized in both UAendo and UA VSM. Immunoblot data demonstrated ovarian hormone specific regulation of ER and ERß protein in UAendo and UA VSM. Compared to luteal phase sheep, both ER and ERß levels in UAendo were elevated in follicular phase sheep. Whereas ERß was elevated by pregnancy in UAendo and UA VSM, ER was not appreciably altered. eNOS was increased in UAendo from follicular and pregnant sheep. Ovariectomized ewes (OVEX) had substantially reduced UAendo ERß, but not UAendo ER or OAendo ER and ERß. In contrast, OVEX increased UA VSM ER and ERß and decreased OA VSM ER and ERß. Treatment with oestradiol-17ß (E2ß), but not progesterone or their combination, increased UAendo ER levels. The reduced ERß in UAendo from OVEX ewes was reversed by E₂ß and progesterone treatment. While ER and eNOS were not elevated in any other reproductive or non-reproductive endothelia tested, ERß was augmented by pregnancy in uterine, mammary, placenta, and coronary artery endothelia. ER and ERß mRNA and protein are expressed in UA endothelium with expression levels depending on the endocrine status of the animal, indicating UA endothelium is a target for oestrogen action in vivo, and that the two receptors appear to be differentially regulated in a spatial and temporal fashion with regard to the reproductive status or HRT.

(Received 25 February 2005; accepted after revision 15 March 2005; first published online 17 March 2005)
Corresponding author R. R. Magness: University of Wisconsin-Madison Medical School, Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Meriter Hospital/Park Atrium-B, 202 S. Park Street, Madison, WI 53715, USA. Email: rmagness{at}wisc.edu

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