When the AT-1 receptor is blocked, the angiosperm II and the rise and metabolite 1-7 activates the AT-2 receptor that plays an important role in remodeling and anti-proliferate effect on cardiac and vascular muscle. These anti-proliferation effects are unique in the sense that this receptor activates several phosphatase interacting with other signaling mechanisms coupled receptors G protein, as well as another class of growth factor receptors in mitochondria. All this becomes relevant, as the disease is characterized by hypertensive left ventricular hypertrophy with a disproportionate increase in interstitial fibrosis and proliferation and hypertrophy of vascular smooth muscle, endothelial dysfunction, macrophage activation (MPC-1 activation) and activation of PDGF-inducing widespread fibrosis and atherosclerosis. A question that arises is whether everything published Yla hypertension is more, to an epiphenomenon of a chronic inflammatory disease, cardiovascular level a? a If this were so, angiotensin II play a central role, which overproduces the formation of peptide or aumentadaa is the expression of the synthesis of AT-1 receptor with a critical decrease of AT-2 receptor which enfermedad.a Seriana responsible for both phenomena could survive. a ANGIOTENSINERGICO SYSTEM IMPACT ON CELLULAR PHYSIOLOGY a Established over 30 years that the angiotensinogen molecule is the limiting cell in the synthesis of tissue angiotensin II. Different proteases, in addition to producing renin angiotensin II (chimasas, dolphins etc.) And the other receivers that are widely distributed polypeptide found externally on the plasma membrane, and intracellular level in the endoplasmic reticulum (ER) and nuclear membrane. Angiotensin receptor AT1 and AT2 have been characterized and cloned.