Our results showed that activation SAPK/JNK and p38MAPK pathways contribute to the maintenance of vasoconstriction to Ang II via AT1 receptors while activation of ERK1/2-eNOS pathway via AT2 receptors in the endothelium contributes to counteracting contraction and decrease the response to Ang II in this experimental model of obesity. The gene discussed is AGTR2; the disease is Obesity.