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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.)

The role of reactive oxygen species in the modulation of the contraction induced by angiotensin II in carotid artery from diabetic rat

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Author(s):
Pernomian, Larissa [1, 2] ; Gomes, Mayara Santos [1] ; Araujo Restini, Carolina Baraldi [3] ; Zambelli Ramalho, Leandra Naira [4] ; Tirapelli, Carlos Renato [5] ; de Oliveira, Ana Maria [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Pharmacol Lab, BR-14040903 Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Pharmacol Lab, BR-14049900 Ribeirao Preto, SP - Brazil
[3] Univ Ribeirao Preto, Dept Med, BR-14096900 Sao Paulo - Brazil
[4] Univ Sao Paulo, Fac Med Ribeirao Preto, Lab Cellular & Mol Pathol, BR-14049900 Ribeirao Preto, SP - Brazil
[5] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, Pharmacol Lab, BR-14040902 Ribeirao Preto, SP - Brazil
Total Affiliations: 5
Document type: Journal article
Source: European Journal of Pharmacology; v. 678, n. 1-3, p. 15-25, MAR 5 2012.
Web of Science Citations: 24
Abstract

The modulation played by reactive oxygen species on the angiotensin II-induced contraction in type I-diabetic rat carotid was investigated. Concentration-response curves for angiotensin II were obtained in endothelium-intact or endothelium-denuded carotid from control or streptozotocin-induced diabetic rats, pre-treated with tiron (superoxide scavenger), PEG-catalase (hydrogen peroxide scavenger), dimethylthiourea (hydroxyl scavenger), apocynin {[}NAD(P) H oxidase inhibitor], SC560 (cyclooxygenase-1 inhibitor), SC236 (cyclooxygenase-2 inhibitor) or Y-27632 (Rho-kinase inhibitor). Reactive oxygen species were measured by flow cytometry in dihydroethidium (DHE)-loaded endothelial cells. Cyclooxygenase and AT1-receptor expression was assessed by immunohistochemistry. Diabetes increased the angiotensin II-induced contraction but reduced the agonist potency in rat carotid. Endothelium removal, tiron or apocynin restored the angiotensin II-induced contraction in diabetic rat carotid to control levels. PEG-catalase, DMTU or SC560 reduced the angiotensin II-induced contraction in diabetic rat carotid at the same extent. SC236 restored the angiotensin II potency in diabetic rat carotid. Y-27632 reduced the angiotensin II-induced contraction in endothelium-intact or -denuded diabetic rat carotid. Diabetes increased the DHE-fluorescence of carotid endothelial cells. Apocynin reduced the DHE-fluorescence of endothelial cells from diabetic rat carotid to control levels. Diabetes increased the muscular cyclooxygenase-2 expression but reduced the muscular AT1-receptor expression in rat carotid. In summary, hydroxyl radical, hydrogen peroxide and superoxide anion-derived from endothelial NAD(P) H oxidase mediate the hyperreactivity to angiotensin II in type I-diabetic rat carotid, involving the participation of cyclooxygenase-1 and Rho-kinase. Moreover, increased muscular cyclooxygenase-2 expression in type I-diabetic rat carotid seems to be related to the local reduced AT1-receptor expression and the reduced angiotensin II potency. (C) 2011 Elsevier B. V. All rights reserved. (AU)

FAPESP's process: 09/01005-0 - Influence of oxidative stress on the response to angiotensin II in contralateral carotid of diabetic rat after balloon-catheter injury
Grantee:Larissa Pernomian
Support Opportunities: Scholarships in Brazil - Doctorate