Endothelium-Dependent Vasodilation Responses in the Patients with Essential Hypertension

Abstract

Background:Patients with essential hypertension have abnormal endothelium-dependent vasodilation due to reduced release of nitric oxide(NO). But it is uncertain whether this defect is selective for some pathways of nitric oxide production or a more generalized abnormality of endothelial function. The purpose of this study was to determine whether this defect is due to an impairment at the specific intracellular signal-transduction pathway level or is a more generalized endothelial dysfunction. Methods and Materials:Forearm blood flow was measured in 10 patients with essential hypertension(mean blood pressure, 129±16.6mmHg;aged 48±10 years old) and 10 control subjects (mean blood pressure, 99.7±6.6mmHg;aged 41±10 years old) using strain-gauge plethys-mography. The endothelium-dependent vasodilators were acetylcholine(7.5, 15, and 30μg/min), which uses a pertussis toxin-sensitive signal transduction pathway, and bradykinin(100, 200, and 400ng/min), which uses a pertussis toxin-insensitive signal transduction pathway to activate nitric oxide production. Sodium nitroprusside(0.8, 1.6, and 3.2μg/min) was used as an endothelium-independent vasodilator. All drugs were infused into the brachial artery and the order was determined randomly. Results:The maximum flow in response to acetylcholine was markedly impaired in hypertensive patients compared with control subjects(5.29±1.86 vs 11.04±2.46ml/min/100ml forearm tissue, p 0.001). But the maximum forearm blood flow in response to bradykinin was similar in the two groups (11.96±3.57 vs 12.48±1.92ml/min/100ml forearm tissue, p=0.69) and that in response to sodium nitroprusside was also similar(10.63±3.74 vs 10.51±2.39ml/min/100ml forearm tissue, p=0.94).