Figure 1. Effect of genetic Mas deficiency or its pharmacological blockade on vascular reactivity.

Vasorelaxant responses to angiotensin-(1–7) [Ang-(1–7); 1 pmol l⁻¹ to 1 mmol l⁻¹; A] and bradykinin (BK; 1 nmol l⁻¹ to 30 μmol l⁻¹; B) in Mas-deficient or wild-type microvessels preincubated with the Mas antagonist A779 (1 μmol l⁻¹). C, after the initial contraction with noradrenaline (NA), the isolated microvessels undergo a spontaneous loss of tension over time, which is similar between wild-type and Mas-deficient segments. Some of the segments used for time control were preincubated with l-NAME (100 μmol l⁻¹). The vasoactive responses are expressed as a percentage of a previous contraction elicited by NA (10 μmol l⁻¹). For each curve, results are shown as means ± SEM of 10–15 mesenteric microvessels from at least 5 different animals. D, acute vasorelaxant effect of a single concentration of Ang-(1–7) (1 μmol l⁻¹) on wild-type and Mas-deficient mesenteric arteries, with and without A779 preincubation. *P < 0.05 vs. wild-type microvessels; †P < 0.05 vs. the respective time control without l-NAME.