The definite mechanisms of AT1-AA-induced hypertension were hitherto not clear; only several possible pathways have been reported, including vasoconstrictor effect in a sustained manner,18 stimulation of vascular smooth muscle cell proliferation and up-regulation of c-fos and c-jun expression,28 causing endothelial dysfunction,8 increasing intracellular calcium,29 stimulating reactive oxygen species (ROS),30 and tissue factor expression.31 The effect of AT1-AA on aldosterone production also has been reported, but the conclusions are inconsistent. Here, FOS is linked to endothelial dysfunction.