on June 11, 2007
Published online before print June 11, 2007, doi: 10.1161/HYPERTENSIONAHA.106.084798
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on January 25, 2007
From the Medizinische Klinik I (P-A.A.-L., K.H., C.D., V.J., T.P.), University of Würzburg, Würzburg, Germany; Integrated Functional Genomics (A.M.M., S.K.), IZKF University of Münster, Münster, Germany; Division of Cardiology (L.N.), University of Manchester, Manchester, United Kingdom; and Schering AG (C.H-H., K.H.F.), Berlin, Germany. * To whom correspondence should be addressed. E-mail: pelzer_t{at}klinik.uni-wuerzburg.de.
Abstract--Experimental and population-based studies indicate that female gender and estrogens protect the cardiovascular system against aldosterone-induced injury. Understanding the function of estrogens in heart disease requires more precise information on the role of both estrogen receptor (ER) subtypes, ER
Revised on February 14, 2007
Both Estrogen Receptor Subtypes,
Paula-Anahi Arias-Loza; 
and 
, Attenuate Cardiovascular Remodeling in Aldosterone Salt-Treated Rats
and ER
. Therefore, we determined whether selective activation of ER or of ER would confer redundant, specific, or opposing effects on cardiovascular remodeling in aldosterone salt-treated rats. The ER agonist 16-LE2, the ER agonist 8-VE2, and the nonselective estrogen receptor agonist 17-estradiol lowered elevated blood pressure, cardiac mass, and cardiac myocyte cross-sectional areas, as well as increased perivascular collagen accumulation and vascular osteopontin expression in ovariectomized rats receiving chronic aldosterone infusion plus a high-salt diet for 8 weeks. Uterus atrophy was prevented by 16-LE2 and 17-estradiol but not by 8-VE2. Cardiac proteome analyses by 2D gel electrophoresis, mass spectrometry, and peptide sequencing identified specific subsets of proteins involved in cardiac contractility, energy metabolism, cellular stress response and extracellular matrix formation that were regulated in opposite directions by aldosterone salt treatment and by different estrogen receptor agonists. We conclude that activation of either ER or ER protects the cardiovascular system against the detrimental effects of aldosterone salt treatment and confers redundant, as well as specific, effects on cardiac protein expression. Nonfeminizing ER agonists such as 8-VE2 have a therapeutic potential in the treatment of hypertensive heart disease.
Key words: aldosterone • estrogen • proteomics • hypertrophy • inflammation
Related Article:
Hypertension 2007 50: 297-298.
This article has been cited by other articles:
 |
|
 |
|
  B. Xue, D. Badaue-Passos Jr, F. Guo, C. E. Gomez-Sanchez, M. Hay, and A. K. Johnson Sex differences and central protective effect of 17{beta}-estradiol in the development of aldosterone/NaCl-induced hypertension Am J Physiol Heart Circ Physiol, May 1, 2009; 296(5): H1577 - H1585. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 J. C. Barbato Estrogen Receptor Activation--Good, Aldosterone Receptor Blockade--Beneficial, Communication Between Receptors...Priceless Hypertension, August 1, 2007; 50(2): 297 - 298. [Full Text] [PDF]
|
|