RESUMO
BACKGROUND:The present study aimed to determine whether there is a regulatory mechanism exerted by endogenous nitric oxide (NO) in the regulation of aquaporin (AQP) water channels in the kidney. METHODS:Male Sprague-Dawley rats were used. They were divided into 4 groups: 1) L-NAME group was treated with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 1 week, 2) indomethacin group was treated with indomethacin (5 mg/kg, twice a day, i.p.) for 2 days, 3) L-NAME/ indomethacin group was treated with L-NAME for 1 week in which indomethacin was cotreated for the last two days, and 4) control group was kept untreated. The abundance of AQP2 and AQP3 proteins was determined in the inner medulla of the kidney. RESULTS:The expression of AQP2 and AQP3 proteins was significantly decreased by indomethacin. L-NAME abolished the indomethacin-induced decreases of AQP channels, although it did not significantly affect the expression of AQP channels by itself. CONCLUSION:These results suggest that endogenous NO system, when stimulated, may downregulate the expression of AQP2 and AQP3 channels in the kidney.