ABNORMAL ENDOTHELIUM-DEPENDENT VASCULAR RELAXATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION

ABNORMAL ENDOTHELIUM-DEPENDENT VASCULAR RELAXATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION
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DOI:
10.1056/nejm199007053230105
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发表时间:
1990-07-05
影响因子:
158.5
通讯作者:
EPSTEIN, SE
EPSTEIN, SE
中科院分区:
医学1区
文献类型:
--
作者:
PANZA, JA;QUYYUMI, AA;EPSTEIN, SE

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内皮通过影响血管平滑肌的收缩活动调节血管张力。内皮对血管的这种调节作用在人类和动物的动脉粥样硬化动脉以及高血压动物模型中被证明是受损的。为了确定原发性高血压患者的血管舒张是否存在内皮依赖性异常,我们研究了18例高血压患者(平均年龄[.+-])前臂血管对乙酰胆碱(内皮依赖性血管扩张剂)和硝普钠(平滑肌直接扩张剂)的反应。[d], 50.7 .+-。10年;10名男性和8名女性)和18名正常对照(平均年龄49.9岁+-)。9;9男9女)。将药物以逐渐增加的浓度注入肱动脉,并通过应变计体积描记术测量前臂血流的反应。患者和对照组的前臂基础血流量相似(平均+-。Sd, 3.4 +-。1.3和3.7.+-。每分钟每100毫升前臂组织0.8毫升;P不显著)。高血压患者对乙酰胆碱的血流反应和血管阻力明显降低(P < 0.0001);前臂最大血流为9.1±。患者每100毫升每分钟5毫升,20.0。对照组为每100毫升每分钟8毫升(P < 0.0002)。然而,血流反应和血管对硝普钠的抵抗之间没有显著差异。由于乙酰胆碱的血管扩张作用也可能是由于肾上腺素能神经末梢对去甲肾上腺素释放的突触前抑制,因此在酚妥拉明诱导的。α期间评估了乙酰胆碱的作用。肾上腺素的封锁。在这些条件下,高血压患者对乙酰胆碱的反应也明显减弱(P < 0.03)。内皮介导的血管舒张在原发性高血压患者中受损。这种缺陷可能在高血压患者中观察到的阻力血管功能异常中起重要作用。
Endothelium regulates vascular tone by influencing the contractile activity of vascular smooth muscle. This regulatory effect of the endothelium on blood vessels has been shown to be impaired in atherosclerotic arteries in humans and animals and in animal models of hypertension. To determine whether patients with essential hypertension have an endothelium-dependent abnormality in vascular relaxation, we studied the response of the forearm vasculature to acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle (in 18 hypertensive patients (mean age [.+-. SD], 50.7 .+-. 10 years; 10 men and 8 women) two weeks after the withdrawal of antihypertensive medications and in 18 normal controls (mean age, 49.9 .+-. 9; 9 men and 9 women). The drugs were infused at increasing concentrations into the brachial artery, and the response in forearm blood flow was measured by strain-gauge plethysmography. The basal forearm blood flow was similar in the patients and controls (mean .+-. SD, 3.4 .+-. 1.3 and 3.7.+-. 0.8 ml per minute per 100 ml of forearm tissue, respectively; P not significant). The responses of blood flow and vascular resistance to acetylcholine were significantly reduced in the hypertensive patients (P < 0.0001); maximal forearm flow was 9.1 .+-. 5 ml per minute per 100 ml in the patients and 20.0 .+-. 8 ml per minute per 100 ml in the controls (P < 0.0002). However, there were no significant differences between the responses of blood flow and vascular resistance to sodium nitroprusside. Because the vasodilator effect of acetylcholine might also be due to presynaptic inhibition of the release of norepinephrine by adrenergic nerve terminals, the effect of acetylcholine was assessed during phentolamine-induced .alpha.-adrenergic blockade. Under these conditions, it was also evident that the responses to acetylcholine were significantly blunted in the hypertensive patients (P < 0.03). Endothelium-mediated vasodilation is impaired in patients with essential hypertension. This defect may play an important part in the functional abnormalities of resistance vessels that are observed in hypertensive patients.