Effects of valsartan or amlodipine on endothelial function and oxidative stress after one year follow-up in patients with essential hypertension.
Endothelial function is impaired in hypertensive patients. Decreased nitric oxide production and increased oxidative stress are involved in this abnormality. The aim of the present study was to evaluate whether endothelial function and oxidative stress differ following long-term antihypertensive treatment with an angiotensin type 1 receptor blocker, valsartan, or a calcium channel blocker, amlodipine, in patients with essential hypertension. Hypertensive patients were treated with valsartan (80-160 mg/day) or amlodipine (5-10 mg/day) for one year (n = 9 for each). The baseline blood pressure was similar between groups, and the magnitude of the decreases in blood pressure did not differ during treatment at three months, six months, or one year. Endothelial function and oxidative stress markers were examined before and after treatment. Endothelial function, assessed by flow-mediated vasodilation, was significantly improved in hypertensive patients treated with valsartan (5.8 +/- 1.2 to 10.7 +/- 1.4 %, p < 0.01) but not in those treated with amlodipine. The percent increase in vasodilation induced by sublingual nitroglycerin did not differ between the two groups. As markers of oxidative stress, urinary excretion of 8-isoprostane and 8-hydroxy-2'-deoxyguanosine was significantly reduced in patients treated with valsartan, but not in those treated with amlodipine. These findings suggest that the treatment of hypertensive patients with valsartan for at least one year improves endothelial function in association with reduced oxidative stress. The improved endothelial function and reduced oxidative stress might be involved in the benefits of anti-hypertensive treatment beyond simply lowering blood pressure, although the effects of treatment with valsartan or amlodipine over a much longer period are unknown.
Hirooka
Yoshitaka
Y
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan. hyoshi@cardiol.med.kyushu-u.ac.jp
Kimura
Yoshikuni
Y
Sagara
Yoji
Y
Ito
Koji
K
Sunagawa
Kenji
K
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D044466:Asian People; D015415:Biomarkers / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D001916:Brachial Artery / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000208:ethnology / Q000503:physiopathology* / Q000652:urine; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D012039:Regional Blood Flow; D013777:Tetrazoles / Q000627:therapeutic use*; D014633:Valine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000068756:Valsartan; D014664:Vasodilation / Q000187:drug effects
D047228:Angiotensin II Type 1 Receptor Blockers; D015415:Biomarkers; D002121:Calcium Channel Blockers; D013777:Tetrazoles; D017311:Amlodipine; C075750:8-epi-prostaglandin F2alpha; D000068756:Valsartan; D000080242:8-Hydroxy-2'-Deoxyguanosine; D015237:Dinoprost; D003849:Deoxyguanosine; D014633:Valine