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. Here, AGTR1 is linked to Obesity.