Oxidative Dna Damage in Newly Diagnosed and Untreated Patients with Isolated High Blood Pressure: The Acute Effect of Olmesartan

OBJECTIVES: Oxidative stress (OS) is the most important common pathway in the pathogenesis of endothelial and vascular damage related with the cardiovascular risk factors. Reactive oxygen species damage the macromolecules and DNA. 8-OHdG (8-hydroxy-2’-deoxyguanosine) is the reliable marker for oxidative DNA damage (ODD). To date, little is known about the presence of OS or ODD in patients with newly diagnosed and untreated primary hypertension (PHT), and the effects of antihypertensives on the ODD. The aims of the study was 1) to determine the oxidative DNA damage and to compare with normotensive healthy persons, 2) to determine the factors related with 8-OHdG level, and 3) to investigate the acute effect of olmesartan on 8-OHdG levels, in patients with newly diagnosed untreated PHT. MATERIAL and METHODS: We enrolled 49 newly diagnosed, never treated, mild to moderate hypertensive patients with no additional cardiovascular or OS risk factors, and age and sex-matched 20 normotensive healthy persons. At the beginning of the study; biochemical tests, glomerular filtration rate measurement, and urinalysis were performed. Echocardiography was performed. 8-OHdG levels were obtained in all subjects. Olmesartan at a dose of 20 or 40 mg/day was administered for 4 weeks. All measurements were repeated after the treatment period. RESULTS: Baseline mean levels of 8-OHdG (6.1±1.0 ng/ml) in patients were significantly higher than the control group (3.8±0.7 ng/ml) (p<0.001). Treatment with olmesartan significantly reduced the 8-OHdG levels independent of the blood pressure lowering effect. Mean levels of 8-OHdG after treatment were higher than the controls (4.6±0.9 ng/ml) (p<0.01). There was no correlation between 8-OHdG levels and demographic and laboratory values. CONCLUSION: ODD is higher in patients with newly diagnosed untreated PHT than normotensive persons, and olmesartan seems to be improve ODD.