Background It has been reported that renovascular hypertensionactivates the reninangiotensin system, leading to anincrease in oxidative stress. We sought to determine whetherrenal-artery angioplasty improves endothelial dysfunction inpatients with renovascular hypertension through a reductionin oxidative stress.
Methods We evaluated the response of forearm blood flow to acetylcholine,an endothelium-dependent vasodilator, and isosorbide dinitrate,an endothelium-independent vasodilator, before and after renal-arteryangioplasty in 15 subjects with renovascular hypertension and15 controls without hypertension who were matched for age andsex. Forearm blood flow was measured with the use of a mercury-filledSilastic strain-gauge plethysmograph.
Results The forearm blood flow in response to acetylcholinewas less in subjects with renovascular hypertension than incontrols, although the forearm blood flow in response to isosorbidedinitrate was similar in the two groups. Angioplasty decreasedsystolic and diastolic blood pressures, forearm vascular resistance,and urinary excretion of 8-hydroxy-2'-deoxyguanosine and serummalondialdehyde-modified low-density lipoprotein (LDL), indexesof oxidative stress. After angioplasty, the mean (±SD)forearm blood flow in response to acetylcholine was increasedin the patients with renovascular hypertension (19.3±6.8vs. 29.6±7.1 ml per minute per 100 ml, P=0.002). Theincrease in the maximal forearm blood flow in response to acetylcholinecorrelated significantly with the decrease in urinary excretionof 8-hydroxy-2'-deoxyguanosine (r=0.51, P=0.004) andserum malondialdehyde-modified LDL (r=0.39, P=0.02).Coinfusion of ascorbic acid (vitamin C) augmented the responseof forearm blood flow to acetylcholine before angioplasty (P<0.001)but not after angioplasty.
Conclusions These findings suggest that excessive oxidativestress is involved, at least in part, in impaired endothelium-dependentvasodilatation in patients with renovascular hypertension.
Source Information
From the First Department of Internal Medicine (Y.H., S.S., K.N., H.M., K.C.) and the Department of Clinical Laboratory Medicine (T.O.), Hiroshima University Faculty of Medicine, Hiroshima, Japan.
Address reprint requests to Dr. Higashi at the Division of Hypertension and Cardiology, First Department of Internal Medicine, Faculty of Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan, or at yhigashi{at}hiroshima-u.ac.jp.
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