The farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily that is expressed in the vasculature; our previous work showed that FXR regulated vascular reactivity through NO mechanism. The underlying mechanism for the regulation of vascular tension by FXR remains unclear. The present work was designed to investigate whether FXR regulates calcium homeostasis in aortic vascular smooth muscle cells (VSMCs). Protein abundances of angiotensin II type 1 and 2 receptors (AT_1R, AT_2R), bradykinin type 1 and 2 receptors (B_1R, B_2R), and the inositol 1,4,5-trisphosphate receptor (IP_3R) were analyzed by Western blotting. Kallikrein activity and bradykinin content were assayed by using spectrophotometry and a bradykinin assay kit, respectively. Aortic contraction, intracellular Ca^(2+) concentrations ([Ca^(2+)]_i), sarco/endoplasmic reticulum Ca^(2+) ATPase (SERCA) activities, and IP_3-evoked Ca^(2+) release were investigated, following FXR activation in the presence or absence of AT_2R and B_2R blockade. We found that the FXR agonists GW4064 and INT-747 increased the protein abundance of AT_2R and B_2R in rat aortic VSMCs. AT_2R blockade with PD123319 reversed the effects of FXR agonists on kallikrein activity, B2_R, and bradykinin levels. Moreover, we found that GW4064 and INT-747 decreased [Ca^(2+)]_i, increased SERCA activity, downregulated IP_3R_1 expression, and attenuated IP_3-induced Ca^(2+) release. These effects were partially reversed by AT_2R and B_2R blockade with PD123319 and HOE140, respectively. Our data suggest that FXR regulates vascular tension by modulating extracellular C^a(2+) influx and intracellular Ca^(2+) release from the sarcoplasmic reticulum via activation of an AT_2R-B_2R pathway in rat aortic VSMCs.