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血管紧张素转换酶抑制而非钙拮抗作用可改善原发性高血压患者肾血管对L-精氨酸的反应。

Angiotensin-converting enzyme inhibition, but not calcium antagonism, improves a response of the renal vasculature to L-arginine in patients with essential hypertension.

作者信息

Higashi Y, Oshima T, Sasaki S, Nakano Y, Kambe M, Matsuura H, Kajiyama G

机构信息

First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.

出版信息

Hypertension. 1998 Jul;32(1):16-24. doi: 10.1161/01.hyp.32.1.16.

DOI:10.1161/01.hyp.32.1.16
PMID:9674632
Abstract

Endothelial function has been shown to be impaired in patients with essential hypertension. The purpose of the present study was to determine whether antihypertensive drug therapy improves impaired endothelium-dependent renal vasorelaxation in essential hypertensive patients without atherosclerosis. We evaluated the effects of intravenous infusion of L-arginine (500 mg/kg given over 30 minutes) on systemic and renal hemodynamics in 27 patients with mild to moderate essential hypertension who were randomly assigned to treatment with either the angiotensin-converting enzyme inhibitor imidapril or the calcium antagonist amlodipine for 12 weeks in a double-blind fashion. After the 12 weeks, the decrease in blood pressure was similar in the imidapril (n=14) and amlodipine (n=13) groups. The increase in renal plasma flow was also similar in both groups. L-Arginine-induced renovascular relaxation was increased by imidapril (renal plasma flow, 9.6+/-5.1% to 14.4+/-7.4%; renal vascular resistance, -10.4+/-8.1% to -16.7+/-9.2%, P<0.05, respectively) but not by amlodipine. Urinary excretion of nitrite/nitrate in response to L-arginine was significantly increased by imidapril (90+/-29% to 134+/-63%, P<0.05) but remained unchanged by amlodipine. These findings suggest that angiotensin-converting enzyme inhibition improves the impaired endothelium-dependent renovascular relaxation in patients with essential hypertension due to the increase in nitric oxide production and that the reduction in blood pressure with a calcium antagonist does not play a major role in the potentiation of L-arginine/nitric oxide-mediated effects.

摘要

原发性高血压患者的内皮功能已被证明存在受损情况。本研究的目的是确定抗高血压药物治疗是否能改善无动脉粥样硬化的原发性高血压患者受损的内皮依赖性肾血管舒张功能。我们评估了静脉输注L-精氨酸(30分钟内给予500mg/kg)对27例轻度至中度原发性高血压患者全身和肾脏血流动力学的影响,这些患者被随机双盲分配接受血管紧张素转换酶抑制剂咪达普利或钙拮抗剂氨氯地平治疗12周。12周后,咪达普利组(n = 14)和氨氯地平组(n = 13)的血压下降情况相似。两组的肾血浆流量增加情况也相似。咪达普利可增强L-精氨酸诱导的肾血管舒张(肾血浆流量,从9.6±5.1%增至14.4±7.4%;肾血管阻力,从 - 10.4±8.1%降至 - 16.7±9.2%,P均<0.05),而氨氯地平则无此作用。咪达普利可使L-精氨酸刺激后的尿亚硝酸盐/硝酸盐排泄显著增加(从90±29%增至134±63%,P<0.05),而氨氯地平对此无影响。这些发现表明,血管紧张素转换酶抑制通过增加一氧化氮生成改善原发性高血压患者受损的内皮依赖性肾血管舒张,而钙拮抗剂降低血压在增强L-精氨酸/一氧化氮介导的效应中不起主要作用。

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