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This study sought to determine if apocynin, a nicotinamide adenine dinucleotide phosphate oxidase inhibitor, would attenuate arterial stiffness in salt-sensitive hypertensive rats via structural and functional changes in conduit arteries. We showed that tail blood pressure was significantly higher in deoxycorticosterone acetate-salt-induced hypertensive (DSH) rats compared with the sham control group (P&lt;0.01). Morphological analysis and biochemical assay showed that large arteries in DSH rats underwent significant remodeling including increased medial thickness in carotid arteries compared with the control rats (194.25±5.66 vs. 120.48±7.93 μm, P&lt;0.05) and increased collagen deposition in thoracic aorta (1.03±0.09 vs. 0.85±0.04 mg cm(-1), P&lt;0.05). These changes were associated with increases in reactive oxygen species (ROS) level and increased thoracic aortic stiffness compared with the control rats (6.21±0.79 m s(-1) vs. 4.64±0.59 m s(-1), P&lt;0.01). Treatment with apocynin significantly prevented ROS increases and collagen deposition (0.84±0.04 vs. 1.03±0.09 mg cm(-1), P&lt;0.05), and reduced arterial stiffness as shown by decreased pulse wave velocity in the thoracic aorta (5.31±0.88 vs. 6.21±0.79 m s(-1), P&lt;0.01). Additionally, apocynin prevented carotid artery wall thickening (58.57±3.40 vs. 78.89±4.10 μm, P&lt;0.05). In conclusion we have shown that increased ROS level is associated with increased aortic stiffness, and deposition of collagen in the aortic arterial wall in DSH rats. Apocynin prevented ROS increases and arterial stiffness in DSH rats. Antioxidant therapy may be a potential treatment of large arterial stiffness in salt-sensitive hypertension.

Anti-stiffness effect of apocynin in deoxycorticosterone acetate-salt hypertensive rats via inhibition of oxidative stress