Intrarenal mas and AT1 receptors play a role in mediating the excretory actions of renal interstitial Angiotensin (1-7) infusion in anaesthetized rats

Abstract

We investigated whether Angiotensin (1-7) induced renal haemodynamic and excretory actions were solely dependent upon intra-renal Mas receptor activation or required functional AT1 receptors. The renin-angiotensin system (RAS) was enhanced by manipulating dietary sodium intake in anaesthetized rats. Angiotensin (1-7) and AT1 and Mas receptor antagonists were infused into the kidney at the cortico-medullary border Mas receptor expression was measured in the kidney. Mean arterial pressure (MAP), urine flow (UF) and fractional sodium excretion (FENa) were 93{plus minus}4 mmHg, 46.1{plus minus}15.7 μL min⁻¹ Kg⁻¹ and 1.4{plus minus}0.3% respectively in the normal sodium group and 91{plus minus}2 mmHg, 19.1{plus minus}3.3 μL min⁻¹ Kg⁻¹ and 0.7{plus minus}0.2% respectively in the low sodium group. Angiotensin (1-7) infusion had no effect on MAP in rats receiving a normal sodium diet but decreased it by 4{plus minus}5% in rats receiving a low sodium diet (P < 0.05). Interstitial Ang (1-7) infusion increased UF by 2 fold and FENa by 3 fold (P < 0.05) in rats receiving a normal sodium diet and to a greater extent, approximately 3 and 4 fold respectively, in low sodium diet rats (both P < 0.05). Angiotensin (1-7) induced increases in UF and FENa were absent in both dietary groups during intra-renal AT1 or Mas receptor inhibition following either Losartan or A-779, respectively. Thus, AT1 receptor activation as well as Mas receptor activation plays an essential role in mediating Ang (1-7) induced natriuresis and diuresis. Whether this is because Ang (1-7) partially antagonizes AT1 receptors or whether Ang (1-7) induced natriuresis is mediated through AT1/Mas receptor dimerization remains unclear.

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