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(Circulation. 1995;91:1732-1738.)
© 1995 American Heart Association, Inc.
Articles |
Impaired Endothelium-Dependent Vasodilation in Patients With Essential Hypertension
Evidence That Nitric Oxide Abnormality Is Not Localized to a Single Signal Transduction Pathway
From the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Correspondence to Dr Julio A. Panza, NIH, Bldg 10, Room 7B-15, Bethesda, MD 20892.
Background Patients with essential hypertension have abnormal endothelium-dependent vascular relaxation, largely related to reduced bioactivity of nitric oxide (NO). The purpose of the present investigation was to determine whether this defect is due to a deficit at the specific intracellular signal-transduction pathway level or is a consequence of a more generalized endothelial abnormality.
Methods and Results The responses of the forearm vasculature to acetylcholine and bradykinin (endothelium-dependent agents that act through different signal transduction pathways) and to sodium nitroprusside (a direct dilator of vascular smooth muscle) were studied in 10 hypertensive patients (5 men, 5 women; aged 48±9 years old [mean±SD]) and 12 control subjects (6 men, 6 women; aged 48±7 years old). To determine the contribution of NO to bradykinin-induced vasodilation, the vascular responses to bradykinin were also measured after administration of NG-monomethyl-L-arginine, an arginine analogue that inhibits the synthesis of NO. Drugs were infused into the brachial artery, and forearm blood flow was measured by strain-gauge plethysmography. The response to acetylcholine was significantly blunted in hypertensive patients (maximal blood flow, 7.5±2 versus 16.6±8 mL · min-1 · 100 mL-1 in control subjects [mean±SD]; P<.005). Similarly, the vasodilator effect of bradykinin was significantly reduced in hypertensive patients compared with control subjects (maximal blood flow, 8.7±2 versus 15.8±6 mL · min-1 · 100 mL-1 in control subjects; P<.005). A significant correlation was found between the maximal blood flow with acetylcholine and that with bradykinin (r=.89). No significant differences were found between the two groups for vascular response to sodium nitroprusside. NG-monomethyl-L-arginine significantly blunted the response to bradykinin in control subjects (maximal blood flow decreased from 15.8±6 to 10.1±2 mL · min-1 · 100 mL-1, P<.003). In contrast, inhibition of NO synthesis did not modify the response to bradykinin in hypertensive patients (maximal blood flow, 8.7±2 and 8.5±3 before and during infusion of NG-monomethyl-L-arginine, respectively; P=NS). As a consequence, the response to bradykinin after inhibition of NO synthesis was not significantly different between the two groups.
Conclusions Patients with essential hypertension have impaired endothelium-dependent vasodilator responses to both acetylcholine and bradykinin. These findings indicate that the endothelial dysfunction in this condition is not related to a specific defect of a single intracellular signal-transduction pathway and suggest a more generalized abnormality of endothelial vasodilator function.
Key Words: endothelium • hypertension • bradykinin • acetylcholine • proteins
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M. Kelm, M. Preik, D. J. Hafner, and B. E. Strauer Evidence for a Multifactorial Process Involved in the Impaired Flow Response to Nitric Oxide in Hypertensive Patients With Endothelial Dysfunction Hypertension, March 1, 1996; 27(3): 346 - 353. [Abstract] [Full Text]
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C. E. Garcia, C. M. Kilcoyne, C. Cardillo, R. O. Cannon III, A. A. Quyyumi, and J. A. Panza Effect of Copper-Zinc Superoxide Dismutase on Endothelium-Dependent Vasodilation in Patients With Essential Hypertension Hypertension, December 1, 1995; 26(6): 863 - 868. [Abstract] [Full Text]
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S. Taddei, A. Virdis, P. Mattei, A. Natali, E. Ferrannini, and A. Salvetti Effect of Insulin on Acetylcholine-Induced Vasodilation in Normotensive Subjects and Patients With Essential Hypertension Circulation, November 15, 1995; 92(10): 2911 - 2918. [Abstract] [Full Text]
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