This Article Full Text Full Text (PDF) All Versions of this Article: 48/3/372    most recent 01.HYP.0000235866.97871.9dv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Reckelhoff, J. F. Search for Related Content PubMed PubMed Citation Articles by Reckelhoff, J. F. Pubmed/NCBI databases Substance via MeSH Related Collections ACE/Angiotension receptors Animal models of human disease Related Article

(Hypertension. 2006;48:372.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Cardiovascular Disease, Estrogen Deficiency, and Inflammatory Cytokines

Jane F. Reckelhoff

From the Department of Physiology and Biophysics, University of Mississippi Medical Center, and the Center for Excellence in Cardiovascular-Renal Research, Jackson, Miss.

Correspondence to Jane F. Reckelhoff, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505. E-mail jreckelhoff@physiology.umsmed.edu

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

The incidence of hypertension increases in women after menopause, as does the susceptibility to myocardial infarction and other cardiovascular diseases.¹ The mechanisms responsible for increased cardiovascular disease risk after menopause are unknown. However, postmenopausal women exhibit increases in inflammatory markers, such as C-reactive protein and inflammatory cytokines, which have been suggested to increase the risk of cardiovascular disease. Arenas et al² report data in this issue of Hypertension that support this hypothesis.

With menopause, the sex hormone levels decrease drastically. Estrogens have been shown to be antioxidative and to modulate both vasoconstrictor and vasodilator systems. For example, estradiol is known to increase NO synthase synthesis and activity³ and to reduce expression of the angiotensin (Ang) type 1 receptor (AT₁R).⁴ Therefore, loss of estrogen production with menopause should be associated with increases in oxidative stress mediated by the renin–Ang system (RAS) because of increased expression of AT₁Rs. This could occur even in the face of no change or lower levels of Ang II with aging. The consequences of increasing oxidative stress would lead to reductions in bioavailable NO because of the increased superoxide production but also the loss of antioxidant capacity. The combination of NO and superoxide produces peroxynitrite, a potent oxidant that is thought to reduce the levels of prostacyclin and increase the levels of thromboxane A2 because of peroxynitrite-mediated protein nitration.¹ Both reactive oxygen species and Ang II are known to upregulate production of inflammatory cytokines, such as tumor necrosis factor (TNF) , by activating nuclear factor . . . [Full Text of this Article]

Related Article:

Tumor Necrosis Factor- and Vascular Angiotensin II in Estrogen-Deficient Rats

Ivan A. Arenas, Stephen J. Armstrong, Yi Xu, and Sandra T. Davidge
Hypertension 2006 48: 497-503. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				N. R. Ferreri Estrogen-TNF interactions and vascular inflammation Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2566 - H2569. [Full Text] [PDF]