Thromboxane-dependent coronary vasoconstriction in obese mice: Role of peroxynitrite

Elisa Villa-Martínez, Selma Romina López-Vaquera, Lesvia Karina Alvarado-Coutiño, Ana María Gámez-Méndez, Amelia Ríos, Bruno Escalante

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Obesity leads to chronic oxidative stress promoting the development of cardiovascular diseases including coronary artery disease and endothelial dysfunction. Increased reactive oxygen species production associated with obesity might lead to endothelial dysfunction through cyclooxygenase (COX) pathway. We evaluated arachidonic acid (AA)-dependent coronary vascular responses and explored COX metabolism in obese C57BL/6 mice. In response to arachidonic acid (AA), isolated hearts from obese mice showed increased vasoconstriction compared with control mice. Released thromboxane (TX) A2 during AA-induced vasoconstriction phase was increased in heart perfusates from obese mice. Indomethacin and 1-benzylimidazole, both reduced vasoconstriction response in control and obese mice. Vasoconstriction response to TXA2 mimetic analog U46619 was 2.7 higher in obese mice. Obesity increased COX-2, TXS and TX receptor protein expression as well as oxidative stress evaluated by nitrotyrosine and peroxynitrite levels, compared with control mice. Obese mice treated with FeTMPyP, a peroxynitrite scavenger, reversed all these parameters to control levels. These data suggest that alterations in COX pathway may be associated with increased generation of free radicals, including peroxynitrite, that result from the oxidative stress observed in obesity.

Original languageEnglish
Article number106631
Pages (from-to)106631
JournalJournal of Lipid Mediators and Cell Signalling
Publication statusPublished - Jun 2022

Bibliographical note

Funding Information:
This work was supported by the Mexican Council for Science and Technology (CONACyT, México, grant number 1180 to BAE). EV, SRLV, and LKAC are fellows from CONACyT, México.

Publisher Copyright:
© 2022 Elsevier Inc.


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