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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress

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Carda, Ana P. P. [1] ; Marchi, Katia C. [2, 1] ; Rizzi, Elen [2] ; Mecawi, Andre S. [3, 4] ; Antunes-Rodrigues, Jose [5] ; Padovan, Claudia M. [6] ; Tirapelli, Carlos R. [1]
Total Authors: 7
[1] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, Farmacol Lab, BR-14040902 Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Farmacol, BR-14040902 Ribeirao Preto, SP - Brazil
[3] Univ Malaya, Fac Med, Dept Physiol, Kuala Lumpur - Malaysia
[4] Univ Fed Rural Rio de Janeiro, Inst Biol, Dept Ciencias Fisiol, Seropedica - Brazil
[5] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Fisiol, BR-14040902 Ribeirao Preto, SP - Brazil
[6] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, Dept Psicol, BR-14040902 Ribeirao Preto, SP - Brazil
Total Affiliations: 6
Document type: Journal article
Web of Science Citations: 15

We hypothesized that acute stress would induce endothelial dysfunction. Male Wistar rats were restrained for 2 h within wire mesh. Functional and biochemical analyses were conducted 24 h after the 2-h period of restraint. Stressed rats showed decreased exploration on the open arms of an elevated-plus maze (EPM) and increased plasma corticosterone concentration. Acute restraint stress did not alter systolic blood pressure, whereas it increased the in vitro contractile response to phenylephrine and serotonin in endothelium-intact rat aortas. NG-nitro-L-arginine methyl ester (L-NAME; nitric oxide synthase, NOS, inhibitor) did not alter the contraction induced by phenylephrine in aortic rings from stressed rats. Tiron, indomethacin and SQ29548 reversed the increase in the contractile response to phenylephrine induced by restraint stress. Increased systemic and vascular oxidative stress was evident in stressed rats. Restraint stress decreased plasma and vascular nitrate/nitrite (NOx) concentration and increased aortic expression of inducible (i) NOS, but not endothelial (e) NOS. Reduced expression of cyclooxygenase (COX)-1, but not COX-2, was observed in aortas from stressed rats. Restraint stress increased thromboxane (TX)B-2 (stable TXA(2) metabolite) concentration but did not affect prostaglandin (PG)F-2 alpha concentration in the aorta. Restraint reduced superoxide dismutase (SOD) activity, whereas concentrations of hydrogen peroxide (H2O2) and reduced glutathione (GSH) were not affected. The major new finding of our study is that restraint stress increases vascular contraction by an endothelium-dependent mechanism that involves increased oxidative stress and the generation of COX-derived vasoconstrictor prostanoids. Such stress-induced endothelial dysfunction could predispose to the development of cardiovascular diseases. (AU)

FAPESP's process: 13/04470-1 - Evaluation of the mechanisms underlying the vascular dysfunction induced by restraint stress
Grantee:Ana Paula Possebon Carda
Support Opportunities: Scholarships in Brazil - Scientific Initiation
FAPESP's process: 13/00808-8 - Consequences of ethanol withdrawal on the vasculature and the systemic and local renin-angiotensin system (ras)
Grantee:Carlos Renato Tirapelli
Support Opportunities: Regular Research Grants