The proposed feedback between angiotensin II AT 2 and AT 1 receptors prompted us to study AT 1 receptor expression in kidneys of male AT 2 receptor-gene disrupted mice ( agtr2 −/y). In wild-type ( agtr2 +/y) mice, AT 1 receptor binding and mRNA is abundant in glomeruli, and AT 1 receptor binding is also high in the inner stripe of the outer medulla. AT 2 receptors are scarce, primarily associated to cortical vascular structures. In agtr2 −/y mice, AT 1 receptor binding and mRNA were increased in the kidney glomeruli, and AT 1 receptor binding was higher in the rest of the cortex and outer stripe of the outer medulla, but not in its inner stripe, indicating different cellular regulation. Although AT 2 receptor expression is very low in male agtr 2 +/y mice, their gene disruption alters AT 1 receptor expression. AT 1 upregulation alone may explain the AT 2 gene-disrupted mice phenotype such as increased blood pressure, higher sensitivity to angiotensin II, and altered renal function. The indirect AT 1 /AT 2 receptor feedback could have clinical significance because AT 1 antagonists are widely used in medical practice.