Intra- renal (IR) Ang (1-7) has diuretic and natriuretic actions that are proportional to the degree of activation of the Renin Angiotensin System (RAS). The question is why the magnitude of this diuresis and natriuresis is compromised in high sodium fed rats (HNa+)(suppressed) RAS and enhanced in low sodium fed rats (LNa+)(activated RAS)? Could the answer lie with changes in IR AT 1 or ‘Mas’ receptor expression? IR Ang (1-7) increased sodium and water excretion in both LNa+ and normal sodium fed rats (NNa+), but the excretory responses were reduced in the presence of the AT1 receptor antagonist (Losartan) and completely blocked by the, ‘Mas’ receptor antagonist (A-779). These data suggest that both AT1 and ‘Mas’ receptors need to be functional in order to fully mediate the renal responses to IR Ang (1-7). The aim of this study was to determine whether there is a relationship between changes in the renal expression of AT1 and ‘Mas’ receptors and the altered responsiveness to IR Ang (1-7) during dietary sodium manipulation. Male Wistar rats (250-300g)(n=4-5) were fed LNa+ (0.03%), NNa+ (0.3%) or HNa+ (3%) for 2weeks. Rats received 1ml Chloralose-Urethane anaesthetic (16.5 and 250 mg/ml, respectively) via the intraperitoneal (IP) route. The right femoral vein was cannulated to facilitate the administration of both sustaining (0.05ml/30mins) and terminal (1.5ml) anaesthesia. The latter was performed after removal of both kidneys. Kidneys were dissected and homogenized. AT1 and ‘Mas’ receptor expression in renal cortex tissue was evaluated using Western blotting and densitometry. Data ±SEM were subjected to a Students t-test and significance was set at (P<0.05). AT 1 receptor expression was increased by 5 fold and reduced by 2 fold in renal cortex tissue of LNa+ and HNa+ rats respectively, (both P<0.05) when compared with rats fed a NNa+ diet. ‘Mas’ receptor expression was the same in all 3 groups. The Ang (1-7) levels in the cortex of LNa+ rats were significantly greater than those in the cortex of NNa+ and HNa+ rats (P<0.05). The current data shows that there is a proportional relationship between AT1 receptor expression in the cortex and the magnitude of the renal actions of IR infused Ang (1-7), which is only partially dependent on the level of ‘Mas’ receptor expression. These data suggest that although the renal tubular responses to IR Ang (1-7), are mediated by the Mas receptor, their magnitude is dependant upon the level of AT1 receptor expression and more specifically Ang II/ AT1 receptor signalling. Thus, in LNa+ rats, IR infused Ang (1-7) acts via the ‘Mas’ receptor to inhibit Ang II/ AT 1 receptor signalling. In HNa+ fed rats the down regulated AT 1 receptor expression implies a reduction in Ang II/AT1 receptor signalling which renders the counter-regulatory effect s of IR infused Ang (1-7) redundant.