Temporary proteinuria occurring after exercise is a common finding, and is explained predominantly by alterations in renal hemodynamics. In this study, it was investigated whether nitric oxide (NO), which is known to be effective on renal hemodynamics and to increase during exercise, has a role in post-exercise proteinuria. At the first step of this study, the effect of acute nitric oxide synthase (NOS) blockage on exercise proteinuria was evaluated. The urinary protein levels in animals, which performed acute exhaustive treadmill running exercise, were considerably elevated compared to the control animals. Significantly elevated urinary protein levels were also detected in animals, which received L-NAME before exhaustion, compared to both control and exhausted groups, and mixed type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, an NO donor (isosorbide mononitrate) was given to rats at one hour before exhaustive exercise. Mixed type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats one hour before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment, on the other hand, in both groups, urinary protein levels were higher than control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications prior to exercise were not different for NO donor and calcium channel blocker groups. These results suggest that, endogenous NO might prevent the post-exercise proteinuria to grow more severe by affecting hemodynamic changes that occur during exercise.