The role of the immune system in the development of hypertension is well-established. Recent studies revealed the critical role of G-protein-coupled receptor signaling, particularly angiotensin II (Ang II) type 1 receptor (AT1R), in immune cell function. Regulator of G-protein signaling (RGS) proteins are critical players in terminating G-protein-coupled receptor signaling, with RGS2 being particularly interesting because it limits signaling downstream of AT1R. Importantly, RGS2 is highly expressed in myeloid immune cells. Global RGS2 deletion results in elevated blood pressure and Ang II-dependent vascular hypercontractility. While evidence supports a key role for RGS2 in vascular tissue, its role in immune cells remains underexplored. Herein, we hypothesized that genetic ablation of RGS2 in myeloid cells would amplify Ang II signaling, thereby exacerbating the inflammatory response to Ang II. To test this hypothesis, we employed a conditional myeloid-specific RGS2 knockout mouse model (RGS2LysM-KO) subjected to chronic Ang II treatment. Contrary to our expectations, both Control and RGS2LysM-KO exhibited comparable changes in blood pressure, cardiac hypertrophy, albuminuria, renal tubular injury markers, vascular dysfunction, and inflammatory profiles in response to Ang II. Altogether, we conclude that myeloid RGS2 does not significantly affect blood pressure nor modulate renal injury or vascular dysfunction effects of Ang II.