Hypertension, or an elevated blood pressure, is the primary modifiable risk factor for cardiovascular disease, the number one cause of mortality worldwide. We previously demonstrated that Th17 activation and interleukin 17A (IL‐17A)/IL‐21 production is integral for the full development of a hypertensive phenotype as well as the renal and vascular damage associated with hypertension. Rho‐associated coiled‐coil containing protein kinase 2 (ROCK2) serves as a molecular switch upregulating Th17 and inhibiting regulatory T cell (Treg) differentiation of CD4+ T cells. Initially, we measured ROCK2 expression and found that ROCK2 is upregulated in splenic and renal CD4+ T cells in hypertensive mice, confirming the potential for influencing hypertension‐associated T cell activation. We then hypothesized that excessive T cell ROCK2 activation, leading to increased Th17/Treg ratios, contributes to hypertension and ultimately, end‐organ damage. We first showed in vitro that KD025, an orally bioavailable ROCK2 inhibitor, inhibits Th17 proliferation and IL‐17A/IL‐21 production. To determine if hypertensive stimuli such as endothelial stretch increase T cell ROCK2 expression, we cultured human aortic endothelial cells exposed to 5% (normotensive) or 10% (hypertensive) stretch with circulating human T cells and HLA‐DR+ antigen presenting cells. Hypertensive stretch increased T cell ROCK2 expression 2‐fold. We then tested the effect of ROCK2 inhibition in vivo on DOCA (deoxycorticosterone) salt‐induced hypertension. DOCA‐salt (uninephrectomy + 100mg DOCA pellet + 1% NaCl drinking water, n=19) was initiated in all animals allowing for hypertension to develop for 10 days, followed by treatment with the ROCK2 specific inhibitor KD025 (50mg/kg i.p. daily starting on Day 11, n=11) for the remainder of the 21‐day protocol. KD025 treatment significantly attenuated cardiac hypertrophy (8.7±0.29 vs 7.6±0.21 mg/grams body weight, p=0.005) and left ventricular (LV) fibrosis (4.9±1.7 vs 2.4±1.3% LV area, p=0.008) by the termination of the study. Flow cytometric analysis revealed that KD025 treatment attenuated renal leukocyte infiltration (414.6±81.5 vs 317.1±43.6 cells/mg tissue, p=0.057) primarily due to an attenuation in the number of CD3+ T cell infiltrates (58.99±5.55 vs 43.45±3.77 cells/mg tissue, p=0.019). Additional studies were performed using the Angiotensin II (Ang II, 490ng/kg/min) model of hypertension which demonstrated that KD025 treatment starting on Day 1 of Ang II infusion significantly blunted the hypertensive response as early as one week of Ang II treatment (139.4±8.5 vs 108±4.8 mmHg systolic blood pressure, p<0.05, n=5‐6). This protection was accompanied by a decreased Th17/Treg ratio (1.66±0.11 vs 1.31±0.13, p=0.029) of renal T cells in vivo, confirming the effects of KD025 observed in the prior in vitro experiments. These data indicate that the ROCK2‐specific inhibitor KD025 may be a novel therapeutic for the treatment of hypertension and the associated tissue damage.