Dysregulation of sodium and/or water reabsorption by the kidney may contribute to hypertension. As chronic sucrose feeding reduces food intake and in consequence of this, the sodium (Na) intake. The objective of the present study was to investigate the role of kidney sodium and water channels on blood pressure increase in sucrose‐fed rats (SC). Wistar rats (150–180g) received, for 30 days, food ad libitum and sucrose solution (20%) (SC =7) or tap water (control group, C =8). The food ingestion was quantified using a metabolic cage and 1 mg of Na was given by gavage for another group of 5 sucrose fed‐rats (SS), also for 30 days (once a day) in order to normalize the sodium ingestion between SS and C. Mean arterial pressure (MAP) was recorded by a Power Lab system. The mRNA expression levels of epithelial sodium channel (ENaC) and water channel protein (AQP2) were analyzed in the cortical kidney tissue by Real Time RT‐PCR technique. MAP increases (P<0.05) in SC (128±1 mmHg) compared to C (102±4 mmHg) rats; MAP was 132±3 mmHg, in SS rats. Compared to C rats the ENaC and AQP2 expression levels were increased (P<0.05) in SC rats (ENaC: SC=1.95±0,19; C=1.03±0,07; AQP2: SC=2.12±0,19, C=1.07±0,10 arbitrary units). However, in SS group the high expression levels of ENaC and AQP2 were reversed (ENaC: 0,74±0,6, AQP2: 0,99±0,12 arbitrary units) but not MAP. Taken altogether, the results presented here indicate that in chronic sucrose fed‐rats the increased MAP is Na‐independent.Supported by FAPESP, CNPq