Accumulation of angiotensin II (Ang II) in tissues is an Ang II-receptor-mediated process. In pigs, acute angiotensin receptor blockade (ARB) reduced the heart-to-plasma ratio of Ang II following acute infusion. However in rats, chronic ARB treatment increased heart Ang II levels, suggesting that a differential response to ARB treatment may exist in the mammalian heart. Furthermore, the changes in heart aldosterone following chronic ARB treatment are not well described. To address the discrepancy in heart Ang II concentrations following ARB treatment, three groups ( n = 6) of rats were chronically studied: (1) control; (2) angiotensin II (Ang II; 80 ng/min for 28 d); and (3) angiotensin II + olmesartan (ARB; 10 mg/kg/d for 21 d). Ang II-infusion increased intracardiac Ang II by 40% (53 ± 2 versus 74 ± 6 fmol/g) and intrarenal Ang II over 2-fold (96 ± 6 versus 207 ± 14 fmol/g), and chronic ARB treatment decreased Ang II by 48% in the heart (50 ± 7 fmol/g) and over two-fold in the kidney (92 ± 7 fmol/g), suggesting that accumulation of Ang II in the heart is receptor-mediated as in the kidney. Ang II increased plasma aldosterone 2.5-fold (1.4 ± 0.1 versus 3.5 ± 1.2 nmol/L) and was exacerbated by ARB treatment (5.6 ± 1.0 nmol/L). Intracardiac aldosterone was exacerbated by ARB treatment (control: 2.2 ± 0.3; Ang II: 2.7 ± 1.1; ARB: 7.8 ± 1.7 pmol/g). Suppression of intracardiac Ang II with ARB is consistent with the existing view of Ang II-receptor-mediated uptake by tissues.