Abstract
Evidence to date suggests that a positive interaction between natriuretic factors promotes sodium excretion to maintain sodium homeostasis and blood pressure. Although the involvement of renal dopamine D1 receptor (D1R) in promoting sodium excretion is well established; the role of Angiotensin (Ang) 1-7 Mas receptor (MasR) is not clear. Here we provide evidence for a functional interaction between these two renal G protein-coupled receptors which suggests that natriuretic response to Ang 1-7 via MasR is dependent on D1R activation. Male Sprague Dawley rats of comparable weight and age were infused with Ang 1-7, MasR antagonist DPro, D1R agonist SKF38393 and D1R antagonist SCH23390. Blood pressure was monitored throughout the experimental procedure and none of the infused drugs affected the pressure. Animals infused with saline alone served as controls. Infusion of Ang1-7 caused significant natriuresis and robust diuresis compared to saline. SKF38393 infusion also induced significant natriuresis and diuresis when compared to saline infusion. Both natriuretic and diuretic response to Ang 1-7 was blocked by Dpro and SCH23390. However, Dpro failed to block SKF38393 response. Concomitant infusion of SKF38393 and Ang 1-7 did not show a cumulative natriuretic or diuretic effect when compared to SKF38393 or Ang 1-7 infusion alone. FENa (%), control (saline): 0.30 ± 0.09; Ang 1-7: 1.03 ± 0.21; Ang 1-7 plus Dpro: 0.49 ± 0.11; Ang 1-7 plus SCH23390: 0.36 ± 0.10; SKF38393: 0.83 ± 0.16; SKF38393 plus SCH23390: 0.41 ± 0.09; SKF38393 plus Dpro: 0.82 ± 0.17; Ang 1-7 plus SKF38393: 1.06 ± 0.21. These data suggest that Ang 1-7 via MasR causes natriuresis which is dependent on D1R activation. On the other hand, renal D1R-mediated sodium excretion is independent of MasR. This study is a paradigm shift as these data identify a novel functional unidirectional interaction between renal MasR and D1R which deviates from commonly known receptor-receptor interaction.
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