The obese Zucker rat reportedly has increased activity of the intra-renal renin-angiotensin-aldosterone system (RAAS), which conceptually could contribute to elevated salt-sensitivity and blood pressure (BP). Our aim was to determine whether there was increased angiotensin II type I receptor (AT1R)-mediated upregulation of expression or activity of the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), and/or the epithelial sodium channel (ENaC) in obese versus lean Zucker rats. Male obese and lean Zucker rats (10-weeks old) were fed either: 1) control chow (1% NaCl) or 2) chow with candesartan (CAN), an AT1R antagonist (25 mg/kg∙diet) for 14 weeks (n = 8/treatment/body type). BP measured by radiotelemetry, was markedly reduced by CAN (approximately 20-25 mm Hg) in both lean and obese rats with no body type differences. Obese rats had significantly greater net natriuretic response to single injections of hydrochlorothiazide and benzamil, suggesting increased activity of NCC and ENaC, respectively; however only the response to benzamil was reduced by CAN. CAN led to a significant reduction in whole kidney levels of NCC and -ENaC (70-kDa band) in both lean and obese rats. However, it significantly increased -ENaC and NKCC2 levels; and these increases were greater in obese rats. These studies suggest that relatively increased ENaC, but not NCC activity, in obese rats is due to enhanced AT1R activity. CAN attenuated the reduction of several renal transporters in the obese rat kidney. Finally, differences in intra-renal AT1R activity do not seem to be responsible for BP differences between lean and obese rats.