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Hypertension. 2006;48:558-559
Published online before print August 28, 2006, doi: 10.1161/01.HYP.0000237771.13491.ce
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(Hypertension. 2006;48:558.)
© 2006 American Heart Association, Inc.


Editorial Commentaries

Aging Modifies the Cardiac Response to Estrogen

A New Dimension to Hormone Replacement Therapy

Carmen Hinojosa-Laborde; Merry L. Lindsey

From the Departments of Anesthesiology (C.H.-L.) and Medicine (M.L.L.), Division of Cardiology, University of Texas Health Science Center, San Antonio, Tex.

Correspondence to Merry L. Lindsey, Medicine/Cardiology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900. E-mail lindseym@uthscsa.edu


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

In this issue of Hypertension, Jazbutyte et al1 introduce the novel idea that aging impairs the ability of the heart to respond to estrogen replacement. Using young (3-month-old) and senescent (24-month-old) spontaneously hypertensive rats (SHRs), they compared the effect of estrogen on cardiac hypertrophy and gene expression in rats given ovariectomy with and without estrogen replacement. They hypothesized that estrogen replacement would differentially alter the cardiac hypertrophic response to ovariectomy. After sham or ovariectomy surgery with and without estrogen replacement, the young and senescent rats were followed for 6 weeks. Blood pressure was elevated in all of the groups and was not affected by estrogen supplementation. Estrogen attenuated the increase in relative heart weight in the ovariectomized young group but not in the senescent group. Cardiac estrogen receptor {alpha} levels were lower in the senescent rats (both intact and ovariectomy groups) compared with the corresponding young groups, and estrogen replacement increased receptor levels. In addition, {alpha} myosin heavy chain levels decreased and ß myosin heavy chain levels increased in all 3 of the senescent groups. In rodents, {alpha} myosin heavy chain is the predominant isoform, and a shift in isoforms is a marker of cardiac hypertrophy.2 Estrogen attenuated the decrease in {alpha} myosin heavy chain in young ovariectomized rats but not senescent rats. Together, these data implicate an age-related loss in cardiac estrogen sensitivity with the development of cardiac hypertrophy. That the same levels of estrogen can have differential effects on the left ventricle depending on the age that replacement is initiated offers . . . [Full Text of this Article]


Related Article:

Aging Reduces the Efficacy of Estrogen Substitution to Attenuate Cardiac Hypertrophy in Female Spontaneously Hypertensive Rats
Virginija Jazbutyte, Kai Hu, Patricia Kruchten, Emmanuel Bey, Sebastian K.G. Maier, Karl-Heinrich Fritzemeier, Katja Prelle, Christa Hegele-Hartung, Rolf W. Hartmann, Ludwig Neyses, Georg Ertl, and Theo Pelzer
Hypertension 2006 48: 579-586. [Abstract] [Full Text] [PDF]



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V. Jazbutyte, P. A. Arias-Loza, K. Hu, J. Widder, V. Govindaraj, C. von Poser-Klein, J. Bauersachs, K.-H. Fritzemeier, C. Hegele-Hartung, L. Neyses, et al.
Ligand-dependent activation of ER{beta} lowers blood pressure and attenuates cardiac hypertrophy in ovariectomized spontaneously hypertensive rats
Cardiovasc Res, March 1, 2008; 77(4): 774 - 781.
[Abstract] [Full Text] [PDF]