Kidneys are organs that participate of long-term arterial pressure regulation.Na + K + -ATPase (NKA) is an integral protein of the plasma membrane that participates in the major transport mechanisms in the renal tubules providing the electrochemistry gradient for the sodium reabsorption, others substrates and fluid.Chronic administration of ouabain (OUA), a NKA inhibitor, induces hypertension in Wistar rats.However, the role of kidneys in this model of hypertension is not elucidated.In this way, the aim of the present study was evaluate the possibles alterations in renal funtion induced by the chronic treatment with OUA by 5 and 20 weeks.For this, male Wistar rats were treated with vehicle (CT) or OUA (~8.0 µg/day, subcutaneously) during 5 or 20 weeks and after the period of treatment animals were placed in metabolic cages to evaluate renal function.As previously demonstrated, chronic treatment with OUA induced hypertension in a similar magnitude in both experimental groups (5 weeks: CT 126 ± 4 vs OUA 147 ± 2 mmHg; 20 weeks: CT 124 ± 2 vs OUA 139 ± 2 mmHg).Moreover, OUA administration was able to increase water intake (OUA 5 weeks: 32%; OUA 20 weeks: 34%), urinary flow (OUA 5 weeks: 62%; OUA 20 weeks: 64%) and protein expression of α 1 isoform of NKA (OUA 5 weeks: 90%; OUA 20 weeks: 70%).However, OUA treatment did not alter significantly the glomerular filtration rate, likewise the fractional excretion of Na + and K + .In summary, chronic OUA treatment induces mild hypertension independent of the period of administration, but the kidneys don't play an important role in the hypertensive process in this model of hypertension.