AT1 and AT2 receptors seem to be mutually antagonistic and the upregulation of AT2 receptor would play a role in the pathogenesis and remodeling of cardiovascular and renal diseases. AT2 receptor is abundantly and widely expressed in fetal tissues, but present at low levels in adult tissues and re-expressed in certain pathological conditions such as vascular injury. The overall cellular effect of AT2 and AT1 receptors co-stimulation is a premature termination of AT1 receptors-elicited cell growth signals by AT2 receptors. Our recent results using AT2 receptor null mice suggest that selective AT1 receptor blockade as well as the stimulation of uninhibited AT2 receptor by angiotensin II is important in the ARB-mediated improvement of cardiovascular remodeling.