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(Circulation Research. 2009;104:141.)
© 2009 American Heart Association, Inc.

Editorials

Cyclooxygenase-2-Derived Prostaglandin F₂

An Endothelium-Derived Contractile Factor Acting Independently of Other Endothelium-Derived Contractile Factors via Vascular Thromboxane Receptors

Karsten Schrör

From the Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Heinrich-Heine-Universität, Germany.

Correspondence to Karsten Schrör, Institut für Pharmakologie und Klinische Pharmakologie, Universitätsklinikum Düsseldorf, Heinrich-Heine-Universität, Moorenstr. 5, D-40225 Düsseldorf, Germany. E-mail karsten.schroer@uni-duesseldorf.de

See related article, pages 228–235

Key Words: EDCF • hamster aorta • PGF₂ • thromboxane receptors

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

Soluble vasoactive factors derived from vascular endothelium modulate the tone of underlying smooth muscle cells. Stimulation of intact, ie, endothelialized, vessels with acetylcholine causes vasodilation by release of endothelium-derived relaxing factors (EDRFs), mostly NO and hyperpolarizing factor(s) (EDHF). The endothelium also produces contractile factors (EDCF) of different origin.¹ Thus, any reduced endothelium-dependent relaxation or even vasoconstriction could result from either loss of EDRFs, (enhanced) generation of EDCFs, or a combination of both. EDCF-mediated vasoconstriction might prevail with increasing age, as well as disturbed endothelial function, for example, in hypertension^1,2 or type 2 diabetes.³ In addition to reduced generation of vasodilator prostaglandins (PGs), such as PGI₂, enhanced production of vasoconstrictor prostanoids has been described.^4,5 Oxygen-derived free radicals and isoprostanes, generated by exaggerated oxidative stress, are further members of the EDCF family. Thus, EDCFs represent an inhomogeneous group of compounds with different chemical identity.

In the few last years, vasocontractile prostanoids, generated by endothelial cyclooxygenase(s) (COX[s]), have come into focus as significant EDCFs.¹ One reason for this is the upregulation of endothelial COXs and enzymes of PG-endoperoxide catabolism during the aging process and hypertension with enhanced generation of these compounds^6,7; another reason is the low selectivity of prostanoids for their membrane receptors. Vasoconstrictor prostanoids act on vascular smooth muscle cells via the thromboxane-prostanoid (TP) receptor.⁸ However, reactive oxygen species and other primary PGs, including PGI₂ at higher concentrations,⁹ may also activate this receptor and cause vasoconstriction.

In this issue of Circulation Research, Wong and colleagues¹⁰ demonstrate generation of a . . . [Full Text of this Article]

Related Article:

Cyclooxygenase-2–Derived Prostaglandin F₂ Mediates Endothelium-Dependent Contractions in the Aortae of Hamsters With Increased Impact During Aging

Siu Ling Wong, Fung Ping Leung, Chi Wai Lau, Chak Leung Au, Lai Ming Yung, Xiaoqiang Yao, Zhen-Yu Chen, Paul M. Vanhoutte, Maik Gollasch, and Yu Huang
Circ. Res. 2009 104: 228-235. [Abstract] [Full Text] [PDF]

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				A. Barac and J. A. Panza Mechanisms of Decreased Vascular Function With Aging Hypertension, June 1, 2009; 53(6): 900 - 902. [Full Text] [PDF]