Effect of nitric oxide on exercise-induced proteinuria in rats

Abstract

Gü ndü z, Filiz, Oktay Kuru, and Ü mit Kemal S entü rk. Effect of nitric oxide on exercise-induced proteinuria in rats. J Appl Physiol 95: 1867-1872, 2003. First published July 18, 2003 10.1152/japplphysiol.00599.2003.-Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received N -nitro-L-arginine methyl ester before exhaustion, compared with 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, a NO donor (isosorbide mononitrate) was given to rats 1 h 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 1 h 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 in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise. nitric oxide synthase; nitric oxide synthase blockage; isosorbide mononitrate; diltiazem NITRIC OXIDE (NO) has an important role in regulation of kidney functions, as well as in the regulation of many other tissues and organs. NO is effective in regulation of glomerular and medullary hemodynamics through vascular resistance, tubuloglomerular feedback response, renin release, and regulation of extracellular fluid volume (16,17). It was demonstrated that acute systemic NO synthase (NOS) blockage causes a prominent increase in resistance of efferent and afferent arterioles and decreases renal blood flow besides increasing the systemic blood pressure (BP) (1). However, glomerular filtration rate either is not affected or is decreased less compared with the renal blood flow, because of the increased filtration fraction after NOS blockade (15,16). In addition, it was shown that NOS blockage affects proximal tubular functions, and decreases total (absolute) and fractional tubular reabs...

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