title: [The role of the selective blocking of angiotensin II receptors in the treatment of cardiovascular diseases].
abstract: Angiotensin II plays an important role in blood pressure control and in water and salt homeosthasis. It is involved in the pathogenesis of hypertension and structural alterations of the vasculature, kidney, and heart, including nephrosclerosis, post infarction remodelling and left ventricular hypertrophy. At least two subtypes of receptors have been identified, angiotensin type 1 (AT1) and type 2 (AT2). The AT1 receptor is responsible for all the known effects of Ang II on blood pressure, osmoregulation, and cell growth and consequently for the contribution to cardiovascular and renal pathology. Research has indicated that the AT1 receptor modulates cardiac and vascular hypertrophy, cellular growth and ventricular remodelling. Evidence suggests that, on the other hand, the AT2 receptor is involved in growth inhibition, inhibits cell proliferation, induces vasodilatation and reverses the AT1 induced hypertrophy. The accumulating evidence appears to demonstrate therefore that the function of these receptor subtypes may exerts opposite effects while stimulated by AngII. The angiotensin receptor antagonists are able to inhibit the renin angiotensin system by blocking selectively the AT1 receptor. It is supposed that AT1 receptor antagonists may provide end organ protection by blocking angiotensin II effects via the AT1 receptor leaving the AT2 receptor unopposed: it is conceivable that the stimulation of AT2 receptors may prevent the hypertropic effects seen in conditions such as LVH, hypertrophy, postinfarction remodeling and repair after injury. For this, the AT1/AT2 selectivity associated to these drugs may be important for their effects and to differentiate them from ACE inhibitors.
authors.affiliation: Ospedale G. Casati, Via Settembrini, 1 20017 Passirana di Rho, MI, Italia.
authors.forename: M
authors.initials: M
authors.lastname: Carnovali
mesh_terms: D000803:Angiotensin I / Q000037:antagonists & inhibitors / Q000502:physiology; D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000502:physiology; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000503:physiopathology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000503:physiopathology; D011945:Receptors, Angiotensin / Q000187:drug effects / Q000502:physiology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000803:Angiotensin I