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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.)

Diabetes confers a vasoprotective role to the neurocompensatory response elicited by carotid balloon injury: Consequences on contralateral carotid tone and blood flow

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Author(s):
Pernomian, Larissa [1] ; Gomes, Mayara S. [1] ; Correa, Fernando M. A. [2] ; Restini, Carolina B. A. [3] ; Ramalho, Leandra N. Z. [2] ; de Oliveira, Ana M. [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, BR-14040903 Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil
[3] Univ Ribeirao Preto, Dept Med, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: European Journal of Pharmacology; v. 708, n. 1-3, p. 124-138, MAY 15 2013.
Web of Science Citations: 7
Abstract

The purpose from this study was to investigate the consequences of sensory neurocompensation to carotid balloon injury in diabetic rats on angiotensin II-induced contraction and basal blood flow in contralateral carotid. Concentration-response curves for angiotensin II and blood flow were obtained in contralateral carotid from non-treated or capsaicin-treated streptozotocin-induced diabetic rats that underwent carotid balloon injury. Diabetes increased angiotensin II-induced contraction and impaired the blood flow in non-operated rat carotid. In diabetic rats, balloon injury led to neointima formation, which reduced the blood flow in ipsilateral carotid. Carotid balloon injury in diabetic rats reduced angiotensin II-induced contraction and restored the blood flow in contralateral carotid when compared to diabetic non-operated rat carotid. Capsaicin inhibited the effects evoked by carotid balloon injury on diabetic rat contralateral carotid. Endothelium removal, PEG-catalase (hydrogen peroxide scavenger) or L-NPA (neuronal nitric oxide synthase, nNOS, inhibitor) increased angiotensin II-induced contraction in contralateral carotid from diabetic operated rats to the levels observed in diabetic non-operated rat carotid. Our findings suggest that carotid balloon injury in diabetic rats elicits a neurocompensation that attenuates the diabetic hyperreactivity to angiotensin II in contralateral carotid by a sensory nerves-dependent mechanism mediated by hydrogen peroxide derived from endothelial nNOS. This sensory mechanism also restored the blood flow in this vessel, compensating the impaired blood flow in diabetic rat ipsilateral carotid. Thus, our major conclusions are that Diabetes confers a vasoprotective significance to the neurocompensation to carotid balloon injury in preventing further damage at carotid cerebral irrigation after angioplasty in diabetic subjects. (C) 2013 Elsevier B.V. All rights reserved. (AU)

FAPESP's process: 12/00640-7 - Study of the consequences of the inflammatory process induced by AT1 receptors during atherosclerosis on the ACE2 - angiotensin-(1-7) - Mas axis in mouse aorta and the involvement of Mas receptors in the vaso- and atheroprotective effects of losartan
Grantee:Larissa Pernomian
Support Opportunities: Scholarships in Brazil - Post-Doctoral
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