The adipose tissue renin-angiotensin system (RAS) is proposed to be a pathophysiological link between adipose tissue dysregulation and metabolic disorders induced by fructose rich diet (FRD). RAS can act intracellularly. We hypothesized that adipocytes nuclear membranes possess angiotensin receptors type 1 and type 2 (AT1R and AT2R) that couple to nuclear signaling pathways and regulate oxidative gene expression under the FRD. We analyzed the effect of nine-week consumption of 10% fructose solution on biochemical parameters, adipocyte morphology and expression of AT1R, AT2R, AT1R-associated protein (ATRAP), NOX4, MMP-9, and MnSOD in adipose tissue of Wistar rats. We detected AT1R and AT2R in nuclear fraction. FRD decreased protein level of nuclear angiotensin receptors, while increased AT1R and decreased AT2R levels were observed at plasma membrane. FRD increased mRNA level of ATRAP, while MnSOD mRNA and protein levels were decreased. No significant differences were observed for MMP9 and NOX4 mRNA levels. These findings coincide with hyperleptinemia, elevated blood pressure and triglyceride level, as well as with unchanged visceral adipose tissue mass and morphology upon FRD. Besides providing evidence for nuclear localization of angiotensin receptors in visceral adipose tissue, this study also points to the different effect of FRD on AT1R expression in different cellular compartments. Elevated blood pressure and decreased antioxidative capacity in visceral fat of fructose fed rats were accompanied by an increased AT1R level in plasma membrane while upregulation of ATRAP and decrease of nuclear membrane AT1R suggest an increase in capacity for attenuation of excessive AT1R signaling and visceral adiposity.