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(Hypertension. 2007;49:1222.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Choreographing the Rapid Vascular Effects of Estrogen

Sorting Out the Partners and the Steps

Ross D. Feldman; Robert Gros

From the Departments of Medicine and of Physiology & Pharmacology, University of Western Ontario, Ontario, Canada and the Cell Biology and Vascular Biology Research Groups, Robarts Research Institute, London, Ontario, Canada.

Correspondence to Dr. Ross D. Feldman, Robarts Research Institute, PO Box 5015, 100 Perth Drive, London, Ontario, Canada, N6A 5K8. E-mail feldmanr@lhsc.on.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The rapid effects of steroids (generally) and estrogen (specifically) have emerged from the fringe of vascular biology to the main stage. Based on a series of observations going back more than half a century, scientists have speculated (mostly to small audiences) that a range of steroids, including estrogen, aldosterone, and glucocorticoids, might have rapid effects on smooth muscle. The report by Traupe and colleagues¹ in this issue of Hypertension is an important next step in this process of discovery: the transition from identification of the pathway to the delineation of the components of the signaling system/receptor(s) involved.

A model in which classical estrogen receptors (ERs) act as transcription factors adequately explains most of the effects of estrogen. These ERs (Er, Er_ß, and Er) are all members of the steroid hormone nuclear receptor subfamily. Estrogen binding mediates a conformational change in these receptors with their consequent dissociation from heat shock protein 90 (hsp90) and ER dimerization. ER receptor dimers then interact with other transcriptional cofactors. The interaction of these receptor complexes with estrogen response elements regulates the target genes mediating the reproductive, developmental, behavioral, skeletal, neural, and cardiovascular effects of steroids. This same signaling pathway has been described for a range of other steroid receptors, including those mediating the effects of mineralocorticoids, glucocorticoids, and androgens.

However, it has become increasingly evident that not all of the effects of estrogen (and other steroids) can be explained by this "genomic" model, especially those processes occurring over a time course too . . . [Full Text of this Article]

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Distinct Roles of Estrogen Receptors and ß Mediating Acute Vasodilation of Epicardial Coronary Arteries

Tobias Traupe, Christoph D. Stettler, Huige Li, Elvira Haas, Indranil Bhattacharya, Roberta Minotti, and Matthias Barton
Hypertension 2007 49: 1364-1370. [Abstract] [Full Text] [PDF]

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