Angiotensin II (Ang II) activates signalling pathways predominantly through the G‐protein‐coupled Ang II type 1 receptor (AT₁R). The regulator of G protein signalling 2 (RGS2) is a negative G protein regulator. We hypothesized that RGS2 deletion changes blood pressure regulation by increasing the response to Ang II. To address this issue, we infused Ang II (0.5 mg kg⁻¹ day⁻¹) chronically into conscious RGS2‐deleted (RGS2^−/−) and wild‐type (RGS2^+/+) mice, measured mean arterial blood pressure and heart rate (HR) with telemetry and assessed vasoreactivity and gene expression of AT_1A, AT_1B and AT₂ receptors. Angiotensin II infusion increased blood pressure more in RGS2^−/− than in RGS2^+/+ mice, while HR was not different between the groups, indicating a resetting of the baroreceptor reflex. Urinary catecholamine excretion was similar in Ang II‐infused RGS2^−/− and RGS2^+/+ mice, indicating a minor role of sympathetic tone for blood pressure differences. Myogenic tone and vasoreactivity in response to Ang II, endothelin‐1 and phenylephrine were increased in isolated renal interlobar arterioles of RGS2^−/− mice compared with RGS2^+/+ mice. The AT_1A, AT_1B and AT₂ receptor gene expression was not different between RGS2^−/− and RGS2^+/+ mice. Our findings suggest that RGS2 deletion promotes Ang II‐dependent hypertension primarily through an increase of myogenic tone and vasoreactivity, probably by sensitization of AT₁ receptors.