Document Detail

Reciprocal relationship between reactive oxygen species and cyclooxygenase-2 and vascular dysfunction in hypertension.
MedLine Citation:
PMID:  22671943     Owner:  NLM     Status:  Publisher    
Aims: This study evaluates a possible relationship between reactive oxygen species (ROS) and cyclooxygenase (COX)-2-derived products in conductance and resistance arteries from hypertensive animals. Angiotensin II infused mice or spontaneously hypertensive rats (SHR) treated with the NAD(P)H Oxidase inhibitor apocynin, the mitochondria-targeted SOD2 mimetic mito-TEMPO, the superoxide dismutase analogue tempol, or the COX-2 inhibitor celecoxib were used. Results: apocynin, mito-TEMPO and celecoxib treatments prevented Angiotensin II-induced hypertension, the increased vasoconstrictor responses to phenylephrine and the reduced acetylcholine relaxation. The NOX-2 inhibitor gp91ds-tat, the NOX-1 inhibitor ML171, catalase and the COX-2 inhibitor NS398, abolished the ex vivo effect of Angiotensin II enhancing phenylephrine responses. Antioxidant treatments diminished the increased vascular COX-2 expression, prostanoids production and/or participation of COX-derived contractile prostanoids and TP receptors in phenylephrine responses, observed in arteries from hypertensive models. The treatment with the COX-2 inhibitor normalized the increased ROS production (O<sub>2</sub><sup>.-</sup> and H<sub>2</sub>O<sub>2</sub>), NAD(P)H Oxidase expression (NOX-1, NOX-4, p22phox) and activity, MnSOD expression and the participation of ROS in vascular responses in both hypertensive models. Apocynin and mito-TEMPO also normalized these parameters of oxidative stress. Apocynin, mito-TEMPO and celecoxib improved the diminished nitric oxide (NO) production and the modulation by NO of phenylephrine responses in the Angiotensin II model. Innovation: This study provides mechanistic evidence of circuitous relationship between COX-2 and ROS products in hypertension. Conclusion: The excess of ROS from NAD(P)H Oxidase and/or mitochondria and the increased vascular COX-2/TP receptor axis act in concert to induce vascular dysfunction and hypertension.
Sonia Martínez-Revelles; M Soledad Avendaño; Ana Belen Garcia-Redondo; Yolanda Alvarez; Andrea Aguado; José Vicente Pérez-Girón; Laura García-Redondo; Vanesa Esteban; Juan M Redondo; María Jesús Alonso; Ana María Briones; Mercedes Salaices
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-6-6
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  -     ISSN:  1557-7716     ISO Abbreviation:  -     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-6-7     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Universidad Autónoma de Madrid, Pharmacology, Madrid, Madrid, Spain;
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