Intrarenal Mas and AT1 receptors play a role in mediating the excretory actions of renal interstitial angiotensin‐(1–7) infusion in anaesthetized rats

New Findings What is the central question of this study? Dietary sodium manipulation alters the magnitude of angiotensin‐(1–7) [Ang‐(1–7)]‐induced natriuresis. The present study sought to determine whether this was related to relative changes in the activity of intrarenal Mas and/or AT1 receptors. What is the main finding and its importance? Angiotensin‐(1–7)‐induced diuresis and natriuresis is mediated by intrarenal Mas receptors. However, intrarenal AT1 receptor blockade also had an inhibitory effect on Ang‐(1–7)‐induced natriuresis and diuresis. Thus, Ang‐(1–7)‐induced increases in sodium and water excretion are dependent upon functional Mas and AT1 receptors. We investigated whether angiotensin‐(1–7) [Ang‐(1–7)]‐induced renal haemodynamic and excretory actions were solely dependent upon intrarenal Mas receptor activation or required functional angiotensin II type 1 (AT1) receptors. The renin–angiotensin system was enhanced in anaesthetized rats by prior manipulation of dietary sodium intake. Angiotensin‐(1–7) and AT1 and Mas receptor antagonists were infused into the kidney at the corticomedullary border. Mas receptor expression was measured in the kidney. Mean arterial pressure, urine flow and fractional sodium excretion were 93 ± 4 mmHg, 46.1 ± 15.7 μl min−1 kg−1 and 1.4 ± 0.3%, respectively, in the normal‐sodium group and 91 ± 2 mmHg, 19.1 ± 3.3 μl min−1 kg−1 and 0.7 ± 0.2%, respectively, in the low‐sodium group. Angiotensin‐(1–7) infusion had no effect on mean arterial pressure in rats receiving a normal‐sodium diet but decreased it by 4 ± 5% in rats receiving a low‐sodium diet (P