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

Autor(es)

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: European Journal of Pharmacology; v. 708, n. 1-3, p. 124-138, MAY 15 2013.
• Citações Web of Science: 7

Resumo

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)

• Processo FAPESP: 12/00640-7 - Estudo das consequências do processo inflamatório induzido por receptores AT1 durante aterosclerose sobre o eixo ECA2 - angiotensina-(1-7) -Mas em aorta de camundongo e da participação de receptores Mas nos efeitos vaso- e ateroprotetores de losartan
• Beneficiário: Larissa Pernomian
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 09/01005-0 - Influência do estresse oxidativo sobre a resposta à angiotensina II em carótida contra-lateral à lesão por catéter-balão de rato diabético
• Beneficiário: Larissa Pernomian
• Modalidade de apoio: Bolsas no Brasil - Doutorado