The renin-angiotensin system (RAS) plays a crucial role in blood pressure control and body fluid homeostasis. Angiotensin-(1–7) (Ang-(1–7)) is an endogenous ligand for the G protein-coupled receptor Mas, which has been shown to have distinct cardiovascular and baroreflex actions compared to angiotensin II (Ang II). This study demonstrates that genetic deletion of the *Mas* gene abolishes the binding of Ang-(1–7) to mouse kidneys and eliminates its antidiuretic action after water loading. Ang-(1–7) binds to *Mas*-transfected cells and induces arachidonic acid release, while *Mas*-deficient aortas lose their Ang-(1–7)-induced relaxation response. These findings confirm that *Mas* is a functional receptor for Ang-(1–7) and provide a molecular basis for its physiological actions. The study also highlights the clinical implications of Ang-(1–7)'s counteraction of Ang II, which may explain the beneficial effects of angiotensin-converting enzyme inhibitors.The renin-angiotensin system (RAS) plays a crucial role in blood pressure control and body fluid homeostasis. Angiotensin-(1–7) (Ang-(1–7)) is an endogenous ligand for the G protein-coupled receptor Mas, which has been shown to have distinct cardiovascular and baroreflex actions compared to angiotensin II (Ang II). This study demonstrates that genetic deletion of the *Mas* gene abolishes the binding of Ang-(1–7) to mouse kidneys and eliminates its antidiuretic action after water loading. Ang-(1–7) binds to *Mas*-transfected cells and induces arachidonic acid release, while *Mas*-deficient aortas lose their Ang-(1–7)-induced relaxation response. These findings confirm that *Mas* is a functional receptor for Ang-(1–7) and provide a molecular basis for its physiological actions. The study also highlights the clinical implications of Ang-(1–7)'s counteraction of Ang II, which may explain the beneficial effects of angiotensin-converting enzyme inhibitors.