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. 2002 Nov;20(11):2239-45.
doi: 10.1097/00004872-200211000-00024.

Obesity increases prostanoid-mediated vasoconstriction and vascular thromboxane receptor gene expression

Tobias Traupe  1 , Matthias Lang, Winfried Goettsch, Klaus Münter, Henning Morawietz, Wilhelm Vetter, Matthias Barton
Affiliations

Obesity increases prostanoid-mediated vasoconstriction and vascular thromboxane receptor gene expression

Tobias Traupe et al. J Hypertens. 2002 Nov.

Abstract

Objectives: Vasoconstrictor prostanoids have been implicated in abnormal vasomotion in atherosclerosis and hypertension.

Method: Using lean and diet-induced obese mice, we investigated whether obesity affects vascular function or expression of genes involved in prostanoid action.

Results: In lean C57BL/6J mice, at high concentrations acetylcholine caused endothelium-dependent contractions in the carotid artery but not in the aorta. Endothelium-dependent contractions to acetylcholine were blocked by the non-selective cyclooxygenase (COX) inhibitors indomethacin and meclofenamate, or a prostaglandin H2/thromboxane A2 receptor antagonist, but not by inhibitors of COX-2, thromboxane synthase or cytochrome P450 monooxygenase. Obesity increased endothelium-dependent contractions to acetylcholine in the carotid artery, and prostanoid-mediated vasoconstriction was now present in the aorta. Similarly, contractions to endothelin-1 were largely blocked by meclofenamate and were increased in the aorta of obese mice. Real-time quantitative polymerase chain reaction analysis of the thromboxane receptor gene in the carotid artery revealed a robust upregulation in obese animals (18-fold, 0.05); in comparison, obesity had a less pronounced effect on thromboxane synthase (2.1-fold increase, 0.05), or preproendothelin-1 gene expression (4.2-fold increase, 0.05).

Conclusions: These data demonstrate that obesity augments prostanoid-dependent vasoconstriction and markedly increases vascular thromboxane receptor gene expression. These changes are likely to promote the development of vascular disease, hypertension and thrombosis associated with obesity.

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