It was noted that according to the intensity of the insult, there is a cascade of pro-apoptotic signals and changes in expression levels of PGC-1alpha, a regulator of mitochondrial biogenesis. The overproduction of angiotensin II at tissue level caused by of AT-1 receptor systemic disorders that are often independent of hypertension. All these effects cause a systemic pathophysiology preferably in the heart, kidney, and most of the arteries and arterioles of the body including the coronary arteries and cerebral arteries. It was recently observed that angiotensin II plays a central role in cardiovascular physiology, as well as neuroendocrine regulation and cell cycle control. By the fact that angiotensin II uses the insulin receptor substrate (IRS-1) to relay signals to different intracellular sites, allowing a biochemical explanation why these two systems interact in both the disease and in healthy patients. Since the on angiotensinergico system activity causes an alteration in intracellular signaling mechanisms of insulin, particularly the nuclear factors involved in gene transcription has been shown in experimental studies both in-vitro and in vivo that the thiazolidinediones (glitazones = ligand selective PPAR-gamma, a subfamily of intracellular receptors that regulate the homeostasis of blood pressure, and metabolism of glucose and lipids) with activity for greater sensitivity insulin, have a common path with the system and have also angiotensinergico an anti-hypertensive and antiateroesclerotico. DIAGNOSIS AND TREATMENT a The mainstay of treatment of hypertension is to prevent vascular stiffness, as well as vascular thrombotic events that the disease entails. In addition to myocardial hypertrophy with predominance of interstitial fibrosis, inflammatory lesions caused renal glomerular and small vessels, particularly in the brain and retinal level.