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C57BL\/6 mice were exposed to concentrated ambient PM<jats:sub>2.5<\/jats:sub> or filtered air for 12 wk followed by a 14-day ANG II infusion in conjunction with fasudil, a Rho kinase antagonist, or placebo treatment. Blood pressure was monitored, followed by analysis of vascular function and ventricular remodeling indexes. PM<jats:sub>2.5<\/jats:sub> exposure potentiated ANG II-induced hypertension, and this effect was abolished by fasudil treatment. Cardiac and vascular RhoA activation was enhanced by PM<jats:sub>2.5<\/jats:sub> exposure along with increased expression of the guanine exchange factors (GEFs) PDZ-RhoGEF and p115 RhoGEF in PM<jats:sub>2.5<\/jats:sub>-exposed mice. Parallel with increased RhoA activation, PM<jats:sub>2.5<\/jats:sub> exposure increased ANG II-induced cardiac hypertrophy and collagen deposition, with these increases being normalized by fasudil treatment. In conclusion, PM<jats:sub>2.5<\/jats:sub> potentiates cardiac remodeling in response to ANG II through RhoA\/Rho kinase-dependent mechanisms. 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