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Apocynin increases the eNOS expression in aortas, increases [NO] and decreases [ROS] in endothelial cells of SHR (1146.4)

NOX enzymes are major source of reactive oxygen species (ROS) in many cellular types. Studies suggest the participation of NOX in hypertension. Previous experiments showed that chronic treatment of SHR with apocynin, a NOX inhibitor, prevents the development of hypertension. The aim of this study was evaluate possible alterations in eNOS (endothelial nitric oxide synthase) expression and ROS and nitric oxide (NO) concentrations in aortas and endothelial cells (EC) of SHR treated with apocynin. Wistar and SHR male rats were treated with apocynin (30mg/Kg/day, p.o.) from 4th to 10th week of life. The animals were sacrificed, the thoracic aorta and endothelial cells were removed. The basal expression of eNOS was lower in SHR aorta than in Wistar aorta. eNOS expression was not altered in aortas of Wistar treated with apocynin, but the treatment increased eNOS expression in SHR aortas when compared to untreated SHR. Aortas from treated or untreated SHR showed increased DHE fluorescence than Wistar aortas. EC of treated SHR showed reduced basal [ROS] than EC of untreated SHR. ACh doesn’t increased [ROS] in EC of SHR, Wistar or treated SHR. Basal [NO] in EC of treated SHR was higher than in EC of untreated SHR and similar to Wistar EC. ACh increased [NO] in EC of treated SHR when compared to Wistar and untreated SHR EC. Apocynin prevents hypertension in SHR and increases the eNOS expression in aortas of SHR. Apocynin increases [NO] and decreases [ROS] in endothelial cells of SHR.