Their amino acid sequence seems to be highly conserved across species and across tissues within a species. AT1 and AT2 receptors share only 34% homology and have distinct signal transduction pathways. AT1 receptors have been localized in the kidney, heart, vascular smooth muscle cells, brain, adrenal gland, platelets, adipocytes, and placenta. AT2 receptors are abundant in the fetus, but their number decreases in the postnatal period. 19 In adult tissues, AT2 receptors are present only at low levels, mainly in the uterus, the adrenal gland, the central nervous system, the heart (cardiomyocytes and fibroblasts), and the kidney. 19 AT2 receptors seem to be re-expressed or upregulated in experimental cardiac hypertrophy, myocardial infarction, and vascular and wound healing. 32–34 As shown in Table 1, all the known clinical effects of angiotensin II are mediated by the AT1 receptor. The physiological role of AT1 receptors is very well documented experimentally and clinically. AT1A receptor knockout mice are characterized by a low blood pressure and high circulating renin levels. 35 These mice were also recently shown to display less left ventricular remodeling and an improved survival after myocardial infarction. 36 The physiological role of the AT2 receptor is only partially understood. In recent years, several new functions have been attributed to AT2 receptors, including inhibition of cell growth, promotion of cell differentiation, and apoptosis. 37–40 Thus, AT2 receptors could have an important role in counterbalancing some of the effects of angiotensin II mediated by AT1 receptors. However, this topic remains a matter of debate because controversial results have been published. 41, 42 More recent data also suggest that AT2 receptors could mediate the production of bradykinin, nitric oxide, and perhaps prostaglandins in the kidney. 43 Additional studies are now needed to confirm these multiple roles of AT2 receptors in humans.