Nitric Oxide and Oxidative Stress in Atherosclerotic Renovascular Hypertension: Effect of Endovascular Treatment

Abstract

Because activation of the renin-angiotensin system leads to an increase in oxidative stress, the authors investigated nitric oxide (NO; nitrite + nitrate), superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) levels and the effect of endovascular treatment on these parameters in patients with atherosclerotic renovascular hypertension. The relationship of NO with blood pressure and renal functional indexes was also investigated. In this prospective cohort study, serum creatinine, NO, SOD, catalase, plasma MDA, urinary microalbumin, and NO levels, and blood pressure were determined in 21 patients with hypertension and unilateral renal artery stenosis caused by atherosclerosis at entry and after 24 hours, 2 weeks, and 6 weeks of endovascular treatment. MDA concentrations decreased 24 hours after intervention and remained low 2 and 6 weeks later. In addition, serum SOD and NO and urine NO levels were increased significantly 24 hours after endovascular treatment and decreased after 2 and 6 weeks. However, serum catalase levels did not differ after the intervention. Blood pressures decreased after treatment. There were no significant differences in urinary microalbumin levels, estimated glomerular filtration rates, and creatinine levels after endovascular treatment. Endovascular treatment decreases oxidative stress and may offer new benefits in the treatment of patients with hypertension associated with renal artery stenosis. The decrease in oxidative stress and/or the upregulation of SOD may increase the bioavailability of NO, which in turn may lead to the rapid hypotensive response.