title: Carvedilol reduces plasma 8-hydroxy-2'-deoxyguanosine in mild to moderate hypertension: a pilot study.
abstract: 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.
authors.affiliation: Department of Internal Medicine,Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Republic of Korea. drjuyong@yahoo.com
authors.forename: Juyong
authors.initials: J
authors.lastname: Lee
authors.forename: Mejeong
authors.initials: M
authors.lastname: Lee
authors.forename: Jeong-Uk
authors.initials: JU
authors.lastname: Kim
authors.forename: Kyung Il
authors.initials: KI
authors.lastname: Song
authors.forename: Yun Seok
authors.initials: YS
authors.lastname: Choi
authors.forename: Sang-Sig
authors.initials: SS
authors.lastname: Cheong
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000378:metabolism; D002227:Carbazoles / Q000627:therapeutic use*; D000077261:Carvedilol; D004249:DNA Damage / Q000187:drug effects; D003849:Deoxyguanosine / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors / Q000097:blood; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011412:Propanolamines / Q000627:therapeutic use*; D012720:Severity of Illness Index
chemical_list: D000959:Antihypertensive Agents; D000975:Antioxidants; D002227:Carbazoles; D011412:Propanolamines; D006852:Hydrochlorothiazide; D000077261:Carvedilol; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002097:C-Reactive Protein; D003849:Deoxyguanosine