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Hypertension. 2005;45:986-990
Published online before print April 18, 2005, doi: 10.1161/01.HYP.0000164569.63160.24
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(Hypertension. 2005;45:986.)
© 2005 American Heart Association, Inc.


Original Articles

Carvedilol Reduces Plasma 8-Hydroxy-2'-Deoxyguanosine in Mild to Moderate Hypertension

A Pilot Study

Juyong Lee; Mejeong Lee; Jeong-Uk Kim; Kyung Il Song; Yun Seok Choi; Sang-Sig Cheong

From Department of Internal Medicine (J.L., M.L., K.I.S., Y.S.C., S.-S.C.) and Department of Clinical Pathology (J-U.K.), Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Republic of Korea.

Correspondence to Juyong Lee, MD, Assistant Professor, Gangneung Asan Hospital, University of Ulsan College of Medicine, 415, Bangdong-ri, Sacheon-myeon, Gangenung-si, Gangwon-do, 210-711, Republic of Korea. E-mail drjuyong{at}yahoo.com

The purpose of this pilot study was to test whether carvedilol has a protective effect against oxidative deoxyribonucleic acid (DNA) damage in human hypertension in vivo. Carvedilol’s antioxidant effect has mostly focused on lipid or amino acid so far. However, there has been no data that carvedilol reduces DNA damage in human hypertension. Never-treated mild to moderate hypertension patients and age- and sex-matched control subjects volunteered for the study. The hypertension subjects were given 12.5 or 25 mg of carvedilol or hydrochlorothiazide orally for 2 months and controls were not given any. Fasting blood samples were collected before and after carvedilol. Plasma highly sensitive 8-hydroxy-2'-deoxyguanosine (hs8-OHdG) and high-sensitivity C-reactive protein (hsCRP) were checked with the samples. There were no statistical differences in clinical characteristics in 3 groups. The hs8-OHdG declined from 9.07±4.23 ng/mL to 5.74±3.89 ng/mL (P=0.002) after carvedilol. However, it did not show significant reduction after hydrochlorothiazide (9.01±3.89 versus 8.23±4.12 ng/mL; P=NS). In the control group, the hs8-OHdG concentration was 3.41±2.03 ng/mL and 3.01±2.65 ng/mL at baseline and 2 months later, respectively (P=NS). The baseline hs8-OHdG levels were higher in hypertension groups compared with control (P=0.000). The hsCRP had no significant difference before and after the tested drugs in 2 hypertension groups (group A: 0.21±0.51 versus 0.19±0.37 mg/dL; group B: 0.20±0.45 versus 0.18±0.42 mg/dL). In conclusion, DNA damage caused by reactive oxygen species occurs more in the hypertension patients than normals. Carvedilol significantly reduces DNA damage in the hypertension patients.


Key Words: antioxidants