This Article Full Text Full Text (PDF) All Versions of this Article: 50/1/37    most recent HYPERTENSIONAHA.107.090803v1 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 Roman, R. J. Articles by Lombard, J. H. Search for Related Content PubMed PubMed Citation Articles by Roman, R. J. Articles by Lombard, J. H. Related Collections Animal models of human disease Hypertension - basic studies Oxidant stress Endothelium/vascular type/nitric oxide Related Article

(Hypertension. 2007;50:37.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Does 20-Hydroxyeicosatetraenoic Acid Contribute to Sex Differences in Cardiovascular Risk by Increasing Oxidative Stress?

Richard J. Roman; Julian H. Lombard

From the Department of Physiology, Medical College of Wisconsin, Milwaukee.

Correspondence to Richard J. Roman, Department of Physiology and Kidney Disease Center, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail rroman@mcw.edu

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

Previous studies have indicated that there are large sex differences in the incidence of hypertension, and the role of androgens in enhancing the risk of cardiovascular disease is well recognized.^1,2 However, the mechanisms by which androgens increase blood pressure are poorly understood. Recent studies have demonstrated that androgen-sensitive forms of hypertension are associated with increased production of 20-hydroxyeicosatetranoic acid (20-HETE) in the kidney and the vasculature.³ However, the role of 20-HETE in this form of hypertension has not been established, because this pathway has both prohypertensive and antihypertensive actions.⁴ At the level of the renal tubule, upregulation of the formation of 20-HETE inhibits sodium transport and opposes the development of hypertension, whereas in the vasculature, 20-HETE is a potent vasoconstrictor that promotes hypertension.

The study of Singh et al⁵ in the current issue explores the role of 20-HETE in the development of endothelial dysfunction and hypertension in rats chronically treated with dihydrotestosterone. The results indicate that that the expression cytochrome P450 4A protein and the production of 20 HETE increase in renal arteries of rats treated with dihydrotestosterone. The increase in vascular 20-HETE production is because of upregulation of the expression of the cytochrome P450 4A8 isoform. The development of hypertension in these studies was associated with the development of endothelial dysfunction, as reflected by an impaired vasodilator response to acetylcholine, increased expression of the gp-91 and gp-47 phox subunits of reduced nicotinamide-adenine dinucleotide phosphate oxidase, and increased superoxide production by the vasculature. More importantly, this study is the first . . . [Full Text of this Article]

Related Article:

Vascular Cytochrome P450 4A Expression and 20-Hydroxyeicosatetraenoic Acid Synthesis Contribute to Endothelial Dysfunction in Androgen-Induced Hypertension

Harpreet Singh, Jennifer Cheng, Huan Deng, Rowena Kemp, Tsuneo Ishizuka, Alberto Nasjletti, and Michal Laniado Schwartzman
Hypertension 2007 50: 123-129. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				D. Gebremedhin, K. Yamaura, and D. R. Harder Role of 20-HETE in the hypoxia-induced activation of Ca2+-activated K+ channel currents in rat cerebral arterial muscle cells Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H107 - H120. [Abstract] [Full Text] [PDF]