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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Angiotensin-converting enzyme inhibition, but not calcium antagonism, improves a response of the renal vasculature to L-arginine in patients with essential hypertension.
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Angiotensin-converting enzyme inhibition, but not calcium antagonism, improves a response of the renal vasculature to L-arginine in patients with essential hypertension.

机译:血管紧张素转换酶的抑制作用,而不是钙拮抗作用,不能改善原发性高血压患者肾血管对L-精氨酸的反应。

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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 nitriteitrate 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-arginineitric oxide-mediated effects.
机译:已显示原发性高血压患者的血管内皮功能受损。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内皮依赖性肾血管舒张受损。我们评估了静脉输注L-精氨酸(30分钟内给予500 mg / kg)对27例轻中度原发性高血压患者的全身和肾脏血流动力学的影响,这些患者被随机分配接受血管紧张素转换酶抑制剂咪达普利治疗或钙拮抗剂氨氯地平以双盲方式治疗12周。 12周后,咪达普利(n = 14)和氨氯地平(n = 13)组的血压下降相似。两组的肾血浆流量增加也相似。咪达普利可增加L-精氨酸诱导的肾血管舒张作用(肾血浆流量,9.6 +/- 5.1%至14.4 +/- 7.4%;肾血管阻力,-10.4 +/- 8.1%至-16.7 +/- 9.2%,分别为P <0.05),但氨氯地平没有。咪达普利可显着增加对L-精氨酸的亚硝酸盐/硝酸盐尿排泄(90 +/- 29%至134 +/- 63%,P <0.05),但氨氯地平保持不变。这些发现表明,由于一氧化氮的产生增加,血管紧张素转换酶抑制作用改善了原发性高血压患者受损的内皮依赖性肾血管舒张功能,并且钙拮抗剂的降压作用并未在增强作用中起主要作用。精氨酸/一氧化氮介导的作用

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