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| Author(s): |
Graziela Neves Hagihara
Total Authors: 1
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| Document type: | Master's Dissertation |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2012-05-29 |
| Examining board members: |
Zuleica Bruno Fortes;
Soraia Kátia Pereira Costa;
Claudia Maria da Penha Oller do Nascimento
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| Advisor: | Zuleica Bruno Fortes |
| Abstract | |
Angiotensin II (AngII) can activate mitogen-activated protein kinases (MAPKs) pathways. We investigated the role of obesity and MAPKs in AngII response in monosodium glutamate-induced obese rats (Ob). Endothelium-intact but not endothelium-denuded mesenteric resistance arteries isolated from Ob exhibited a lower response to AngII. The response to nordrenaline and potassium chloride were unaltered. Increased expression of AT2 receptor, nitric oxide synthase (eNOS) and ERK1/2 might be involved in the reduced response since inhibition of AT2R, eNOS and ERK1/2 corrected it. Increased activation of ERK 1/2 in Ob might activate eNOS, generating more NO and vasodilation that contributed to reduce the contraction to AngII. We concluded that, in obesity, the lower response to AngII might be an adaptive mechanism against the increased activation of the renin-angiotensin system. This mechanism involves the participation of the endothelium through a greater release of NO, increased AT2R, eNOS and ERK1/2 expressions. (AU) | |
| FAPESP's process: | 10/03642-5 - Angiotensin II response in resistance mesenteric arteries in obesity: role of MAPKs |
| Grantee: | Graziela Neves Hagihara Abe |
| Support Opportunities: | Scholarships in Brazil - Master |