Effects of carvedilol on oxidative stress in polymorphonuclear and mononuclear cells in patients with essential hypertension.
OBJECTIVE
To compare the effects of carvedilol and propranolol on oxidative stress in leukocytes and C-reactive protein levels in patients with hypertension.


METHODS
Sixty hypertensive patients were randomly assigned to carvedilol (20 mg; n = 30) or propranolol (60 mg; n = 30) for 6 months. Thirty normotensive subjects who were given placebo served as controls. Oxidative stress in polymorphonuclear cells and mononuclear cells were measured by gated flow cytometry. C-reactive protein levels were measured by immunonephelometric assay.


RESULTS
Oxidative stress in polymorphonuclear cells and mononuclear cells was increased significantly in hypertensive patients compared with in normotensive controls. After 6 months of treatment, carvedilol decreased oxidative stress significantly in polymorphonuclear cells by a mean of 45 arbitrary units (95% confidence interval [CI]: 32 to 59 arbitrary units; P <0.001) and propranolol decreased oxidative stress significantly by 20 arbitrary units (95% CI: 7 to 33 arbitrary units; P <0.003; P = 0.001 for difference between treatments). Carvedilol also decreased oxidative stress significantly in mononuclear cells by 23 arbitrary units (95% CI: 15 to 31 arbitrary units; P <0.001), whereas propranolol decreased oxidative stress by 2 arbitrary units (95% CI: 7 to 12 arbitrary units; P = 0.62; P = 0.002 for difference between treatments). Carvedilol decreased C-reactive protein levels significantly by a median of 0.073 mg/dL (interquartile range, 0.034 to 0.112 mg/dL; P <0.001), whereas propranolol decreased levels by 0.012 mg/dL (interquartile range, 0.009 to 0.032 mg/dL; P = 0.26; P = 0.003 for difference between treatments).


CONCLUSIONS
These findings suggest that carvedilol inhibits oxidative stress in polymorphonuclear and mononuclear cells, as well as lowers C-reactive protein levels, to a greater extent than does propranolol in hypertensive patients.
Yasunari
Kenichi
K
Department of General Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan. yasunari@osaka.med.or.jp
Maeda
Kensaku
K
Nakamura
Munehiro
M
Watanabe
Takanori
T
Yoshikawa
Junichi
J
Asada
Akira
A
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D002227:Carbazoles / Q000627:therapeutic use*; D000077261:Carvedilol; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D005260:Female; D006442:Glycated Hemoglobin / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007564:Japan; D007963:Leukocytes, Mononuclear / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D011412:Propanolamines / Q000627:therapeutic use*; D011433:Propranolol / Q000627:therapeutic use; D012307:Risk Factors; D013223:Statistics as Topic; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D015415:Biomarkers; D002097:C-Reactive Protein; D002227:Carbazoles; D000077261:Carvedilol; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006442:Glycated Hemoglobin; D007328:Insulin; D011412:Propanolamines; D011433:Propranolol; D014280:Triglycerides