Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2006;48:994-1001
Published online before print September 25, 2006, doi: 10.1161/01.HYP.0000242482.57186.e8
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
48/5/994    most recent
01.HYP.0000242482.57186.e8v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Arias-Loza, P. A.
Right arrow Articles by Pelzer, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Arias-Loza, P. A.
Right arrow Articles by Pelzer, T.
Related Collections
Right arrow Hypertrophy
Right arrow Receptor pharmacology
Right arrow Animal models of human disease
Right arrow Gene expression
Right arrow Hypertension - basic studies
Right arrow Physiological and pathological control of gene expression

(Hypertension. 2006;48:994.)
© 2006 American Heart Association, Inc.


Original Articles

Medroxyprogesterone Acetate But Not Drospirenone Ablates the Protective Function of 17ß-Estradiol in Aldosterone Salt-Treated Rats

Paula Anahi Arias-Loza; Kai Hu; Andreas Schäfer; Johann Bauersachs; Thomas Quaschning; Jan Galle; Virginija Jazbutyte; Ludwig Neyses; Georg Ertl; Karl-Heinrich Fritzemeier; Christa Hegele-Hartung; Theo Pelzer

From the Medizinische Klinik I (P.A.A.-L., K.H., A.S., J.B., T.Q., J.G., V.J., G.E., T.P.), University of Würzburg, Würzburg, Germany; Schering AG Berlin (K.-H.F., C.H.-H.), Berlin, Germany; and the Division of Cardiology (L.N.), University of Manchester, Manchester, United Kingdom.

Correspondence to Theo Pelzer, Medizinische Klinik I, University of Würzburg, Josef-Schneider Str 2, D-97080 Würzburg, Germany. E-mail pelzer_t{at}medizin.uni-wuerzburg.de

Controversial results obtained from human and animal studies on the prevention of heart disease by estrogens and progestins warrant a better understanding of nuclear hormone receptor function and interaction. To address this issue and taking into account that effects of synthetic progestins are not only referable to action through the progesterone receptor but may also be mediated by other steroid receptors, we characterized cardiovascular function and inflammatory gene expression in aldosterone salt-treated rats on long-term administration of 17ß-estradiol, medroxyprogesterone acetate, and drospirenone, a new progestogen exhibiting antimineralocorticoid activity. The complex pattern of cardiovascular injury in ovariectomized Wistar rats induced by chronic aldosterone infusion plus a high-salt diet was significantly attenuated in sham-ovariectomized rats and by coadministration of 17ß-estradiol in ovariectomized animals after 8 weeks of continuous treatment. The beneficial role of 17ß-estradiol on blood pressure, cardiac hypertrophy, vascular osteopontin expression, perivascular fibrosis, and impaired NO-dependent relaxation of isolated aortic rings was completely abrogated by coadministration of medroxyprogesterone acetate. In contrast, drospirenone was either neutral or additive to 17ß-estradiol in protecting against aldosterone salt-induced cardiovascular injury and inflammation. The current results support the hypothesis of complex interactions among estrogen, progesterone, glucocorticoid, androgen, and mineralocorticoid receptor signaling in cardiovascular injury and inflammation. Novel progestins, such as drospirenone, confer superior effects compared with medroxyprogesterone acetate in a model of aldosterone-induced heart disease because of its antimineralocorticoid properties.


Key Words: aldosterone • estrogen • medroxyprogesterone-acetate • cardiac hypertrophy




This article has been cited by other articles:


Home page
EndocrinologyHome page
C. Otto, I. Fuchs, H. Altmann, M. Klewer, A. Walter, K. Prelle, R. Vonk, and K.-H. Fritzemeier
Comparative Analysis of the Uterine and Mammary Gland Effects of Drospirenone and Medroxyprogesterone Acetate
Endocrinology, August 1, 2008; 149(8): 3952 - 3959.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
T.-M. Lee, M.-S. Lin, and N.-C. Chang
Physiological Concentration of 17{beta}-Estradiol on Sympathetic Reinnervation in Ovariectomized Infarcted Rats
Endocrinology, March 1, 2008; 149(3): 1205 - 1213.
[Abstract] [Full Text] [PDF]


Home page
Hum ReprodHome page
T. Simoncini, X-D. Fu, A. Caruso, S. Garibaldi, C. Baldacci, M.S. Giretti, P. Mannella, M.I. Flamini, A.M. Sanchez, and A.R. Genazzani
Drospirenone increases endothelial nitric oxide synthesis via a combined action on progesterone and mineralocorticoid receptors
Hum. Reprod., August 1, 2007; 22(8): 2325 - 2334.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
P.-A. Arias-Loza, K. Hu, C. Dienesch, A. M. Mehlich, S. Konig, V. Jazbutyte, L. Neyses, C. Hegele-Hartung, K. Heinrich Fritzemeier, and T. Pelzer
Both Estrogen Receptor Subtypes, {alpha} and {beta}, Attenuate Cardiovascular Remodeling in Aldosterone Salt-Treated Rats
Hypertension, August 1, 2007; 50(2): 432 - 438.
[Abstract] [Full Text] [PDF]