一项比较依普沙坦和依那普利对高血压患者血压、血小板和内皮功能影响的双盲随机试验。

Hsin-Bang Leu, Ming-Ji Charng, Philip Yu-An Ding
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引用次数: 29

摘要

肾素-血管紧张素系统是高血压、动脉粥样硬化和许多其他心血管疾病发展的主要因素。血管紧张素II是该系统的主要效应物之一,参与高血压的发病机制,并在单核细胞、血小板和内皮细胞的相互作用中发挥重要作用。血管紧张素转换酶抑制剂或血管紧张素受体拮抗剂对血小板和内皮功能的影响尚不清楚。在一项为期10周的双盲、随机、前瞻性试验中,42名患者(27名男性,15名女性)服用依那普利(10- 20mg /天)或依普罗沙坦(400- 800mg /天)。通过测量血小板因子4 (PF-4)、β -血小板球蛋白(β - tg)、血小板因子4与β -血小板球蛋白的比值来评估血小板活化,通过测量血浆总硝酸盐水平、血管性血友病因子(vWF)水平来评估内皮功能,并通过静脉闭塞性体积描记仪来评估血流。用依那普利或依泊沙坦治疗10周后,依那普利组(从152.2 +/- 18.7 mmHg降至141.9 +/- 23.5 mmHg, P < 0.05)和依泊沙坦组(从151 +/- 10.0 mmHg降至142.3 +/- 12.9 mmHg, P < 0.05)的坐位血压均显著降低。依泊沙坦组舒张压(DPB)显著降低(从94 +/- 8.7降至84.5 +/- 9.6 mmHg, P < 0.05),舒张压降低效果更明显(依泊沙坦组为63%,依那普利组为25%)。此外,在接受大剂量依普沙坦和依那普利治疗的患者中,血小板活化和内皮功能障碍指数呈剂量依赖性降低,这些药物的有益效果与使用这两种药物的血压降低无关。依普沙坦治疗中中度高血压有效且耐受性良好,且依普沙坦对舒张反应的降低效果优于依那普利。大剂量依泊沙坦或依那普利均可显著降低高血压患者血小板活化和内皮功能障碍指标。这两种药物的益处不能仅仅通过它们的降压作用来解释,可能是通过它们对血管紧张素阻断的独特作用来介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A double blind randomized trial to compare the effects of eprosartan and enalapril on blood pressure, platelets, and endothelium function in patients with essential hypertension.

The renin-angiotensin system is the major contributor to development of hypertension, atherosclerosis, and many other cardiovascular diseases. Angiotensin II, one of the main effectors of this system, contributes to the pathogenesis of hypertension and plays an important role in monocyte, platelet, and endothelium interactions. The effects on platelet and endothelial function, either by angiotensin converting enzyme inhibitors or angiotensin receptor antagonists, are still not well understood. A double-blind, randomized, prospective trial of either enalapril (10-20 mg daily) or eprosartan (400-800 mg daily) over a 10-week period was conducted in 42 patients (27 males, 15 females). Platelet activation was evaluated by measuring platelet factor 4 (PF-4), beta-thromboglobulin (beta-TG), the ratio of platelet factor 4 to beta-thromboglobulin, and endothelial function by measuring total plasma nitrate levels, von Willebrand factor (vWF) levels, and blood flow using venous occlusive plethysmography. After a 10-week treatment with enalapril or eprosartan, the sitting blood pressure in both the enalapril group (from 152.2 +/- 18.7 mmHg to 141.9 +/- 23.5 mmHg, P < 0.05) and eprosartan group (from 151 +/- 10.0 mmHg to 142.3 +/- 12.9 mmHg, P < 0.05) was significantly reduced. Significant diastolic blood pressure (DPB) reduction (from 94 +/- 8.7 to 84.5 +/- 9.6 mmHg, P < 0.05) and a greater DBP reduction response were found in the eprosartan group (63% in eprosartan versus 25% in enalapril). Additionally, dose-dependent reductions in the indices of platelet activation and endothelial dysfunction were observed in patients administered high dose treatments of eprosartan and enalapril, and the beneficial effects of these agents were not correlated with the reduction of blood pressure using both agents. Eprosartan is effective and well-tolerated in the treatment of mid-to-moderate hypertension, and the DBP response reduction to eprosartin was better than that to enalapril. A high dose of either eprosartan or enalapril significantly decreased the indices of platelet activation and endothelial dysfunction in hypertensive patients. The benefits of both agents cannot be explained solely by their antihypertensive effects and possibly may be mediated through their unique effect on angiotensin blockade.

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