Pressure Promotes Angiotensin II–Mediated Migration of Human Coronary Smooth Muscle Cells Through Increase in Oxidative Stress

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Abstract
Angiotensin II–mediated oxidative stress may play a role in the pathogenesis of coronary atherosclerosis. We examined the effects of pressure on the angiotensin II–mediated increase in oxidative stress and migration of cultured human coronary smooth muscle cells (SMCs). Increased pressure (100 mm Hg) by helium gas for 48 hours increased angiotensin II–mediated oxidative stress as evaluated by flow cytometry and SMC migration (from 15.9±2.2 to 32.0±2.4 cells per 4 high-power fields, P P N -acetylcysteine (100 mmol/L) but not PD123319 (1 μmol/L) also blocked pressure-induced increases in angiotensin II–mediated oxidative stress and SMC migration ( P <0.05, n=8). These findings suggest a novel cellular mechanism whereby pressure regulates the angiotensin II–mediated migration of SMCs, possibly via angiotensin II type 1 receptors, and which involves PLD-mediated, PKC-mediated, and NADPH oxidase–mediated increases in oxidative stress.