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HAGIHARA GN. Differential participation of MAPKs in angiotensin II-induced contraction in obesity. [Master thesis (Pharmacology)] São Paulo: Instituto de Ciências Biomédicas da Universidade de São Paulo, 2012. Obesity is associated to vascular dysfunction. One of the mechanisms involved in this alteration is increased activation of the renin-angiotensin system, compromising the response to angiotensin II (Ang II), a vasoactive peptide that can activate the mitogen-activated protein kinases (MAPKs) pathways. To investigate the role of obesity and MAPKs in vascular reactivity to Ang II, Wistar rats received monosodium glutamate injections (4.0g/kg, s.c.) from 2 to 6 day after birth and were used at the age of 16 weeks. This treatment was effective in inducing obesity characterized by increased Lee`s index, retroperitoneal and periepididymal fat with no change in lean body mass (soleus and EDL), and induced hypertriglyceridemia, increased VLDL and LDL fractions, with no change in total cholesterol, HDL-cholesterol and systolic blood pressure. The response to Ang II was analyzed in isolated mesenteric resistance arteries using a wire myography. The obese rats had lower response to Ang II when compared to controls. This alteration was endothelium-dependent and involved the AT2 receptor (AT2R) because the AT2R antagonism corrected the lower response. The AT1R protein expression did not differ from controls, while AT2R expression was increased in obese rats. Inhibition of nitric oxide synthase by L-NAME corrected the response to Ang II, indicating the participation of NO in the lower response, which was confirmed by the increased basal expression of eNOS. Inhhibition of NADPH oxidase by apocynin reduced the contraction to Ang II in both groups, indicating that the alteration observed in obese rats did not involve the participation of reactive oxygen species. Because the inhibition of ERK1/2 corrected the Ang II response, we concluded that the lower response to Ang II involves ERK1/2 pathway that promotes vasodilatation. We have also demonstrated that obese rats have increased ERK1/2 expression in basal and Ang II stimulus. Since the inhibition of JNK and p38 MAPKs pathways decreased even more the Ang II response, we concluded that they are involved in maintenance of the contractile response to this agonist. The alterations were specific because there was no difference in the contractile response to norepinephrine and potassium chloride. The MAPKs appear not to be the main

Resposta à angiotensina II em artérias mesentéricas de resistência na obesidade: participação das MAPKs.