Chronic exposure to cold causes arterial hypertension [cold-induce hypertension (CIH)]. Emerging data have indicated that gut barrier dysfunction is involved in the pathogenesis of hypertension. In this study, we explored the effect of gut barrier dysfunction on vascular inflammation induced by cold exposure and the therapeutic effect of atorvastatin in a CIH rat model. The CIH was established by cold exposure for 2 weeks. Two groups of Sprague Dawley rats were exposed to moderate cold (4 ± 1°C), whereas the control group was maintained at room temperature (23 ± 1°C) (10 rats/group). The 2 groups received atorvastatin or vehicle at the beginning of cold exposure, respectively, for 2 weeks. Cold exposure increased mean arterial pressure compared with room temperature group, indicating that animals developed arterial hypertension. Cold exposure induced vascular dysfunction due to decreasing phosphorylated endothelial nitric oxide synthase protein expression in aorta, and these were blunted by atorvastatin. Cold exposure increased the levels of gut-derived inflammatory cytokines, tumor necrosis factor-α, and interleukin-6 production in aorta and resulted in vascular inflammation, whereas atorvastatin prevented these effects. Cold exposure also increased gut permeability, inhibited tight junction protein expression in proximal colon, and resulted in gut barrier dysfunction. Interestingly, atorvastatin eliminated increasing gut permeability, decreasing tight junction protein expression, and gut pathology and reversed gut barrier dysfunction. Atorvastatin attenuated CIH and improved gut barrier function; the beneficial effects might be via inhibiting gut-derived inflammatory cytokines and reversing cold-induced vascular inflammation, suggesting that gut barrier dysfunction may be involved in the pathogenesis of CIH.