Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2002;40:448-450
Published online before print September 3, 2002, doi: 10.1161/01.HYP.0000033465.65961.07
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
40/4/448    most recent
01.HYP.0000033465.65961.07v1
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 arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jackson, E. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jackson, E. K.
Related Collections
Right arrow ACE/Angiotension receptors
Right arrow Cell signalling/signal transduction
Right arrow Smooth muscle proliferation and differentiation
Right arrow Mechanism of atherosclerosis/growth factors

(Hypertension. 2002;40:448.)
© 2002 American Heart Association, Inc.


Editorial Commentary

Commentary on Liu et al

Effect of Estrogen and AT1 Receptor Blocker on Neointima Formation

Edwin K. Jackson

From the Center for Clinical Pharmacology, Departments of Medicine and Pharmacology, University of Pittsburgh Medical Center, Penn.

Correspondence to Edwin K. Jackson, Center for Clinical Pharmacology, University of Pittsburgh School of Medicine, 626 Scaife Hall, 3550 Terrace St, Pittsburgh, PA 15261. E-mail edj+@pitt.edu


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

Epidemiological studies demonstrate sexual dimorphism with respect to arterial blood pressure, incidence of vascular disease, and the rate of progression of renal disease. In this regard, in men age <60 years, arterial blood pressure is higher compared with that of age-matched women, and the incidence of coronary artery disease is 50% less in premenopausal women compared with age-matched men. Decline of kidney function in patients with chronic renal disease is slowed in premenopausal women compared with age-matched men.

After the loss of ovarian function, sexual dimorphisms vis-à-vis hypertension, vascular disease, and rate of progression of kidney disease are no longer present. Arterial blood pressure increases in postmenopausal women, and the incidence of vascular disease and the rate of progression of renal disease equalizes between men and women.

The association of loss of ovarian function and disappearance of sexual dimorphism with respect to hypertension and vascular and renal disease suggests that 17ß-estradiol, the major estrogen produced by the human ovary, may importantly participate in the relative protection afforded to premenopausal women. The conclusion that 17ß-estradiol protects against hypertension, vascular damage, and progression of renal disease is corroborated by animal studies demonstrating antihypertensive, vasculoprotective, and renoprotective effects of 17ß-estradiol.

Like 17ß-estradiol, inhibitors of the renin-angiotensin system, such as ACE inhibitors or angiotensin receptor blockers (ARBs), also reduce blood pressure, protect blood vessels against vascular injury, and have renoprotective effects. Whether these beneficial effects of inhibitors of the renin-angiotensin system are nonadditive, additive, or synergistic with 17ß-estradiol is a critically important question that . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
M. Wang, W. Zhang, P. Crisostomo, T. Markel, K. K. Meldrum, X. Y. Fu, and D. R. Meldrum
Sex differences in endothelial STAT3 mediate sex differences in myocardial inflammation
Am J Physiol Endocrinol Metab, September 1, 2007; 293(3): E872 - E877.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
Y. Xu, H. Arai, X. Zhuge, H. Sano, T. Murayama, M. Yoshimoto, T. Heike, T. Nakahata, S.-i. Nishikawa, T. Kita, et al.
Role of Bone Marrow-Derived Progenitor Cells in Cuff-Induced Vascular Injury in Mice
Arterioscler Thromb Vasc Biol, March 1, 2004; 24(3): 477 - 482.
[Abstract] [Full Text]