高血压患者血管重构和内皮功能:抗高血压治疗的效果。

E L Schiffrin
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引用次数: 34

摘要

目的:回顾抗高血压药物对高血压患者和实验性高血压模型中小动脉(阻力大小)结构和功能改变的影响,因为这些血管可能导致血压升高或高血压并发症。主要观察指标:高血压患者的小动脉的结构和内皮依赖性舒张是通过臀皮下活检获得的,高血压大鼠的不同血管床,没有和经过降压治疗,并在钢丝肌图上或作为加压动脉进行研究,在不同的研究中被描述。结果:血管紧张素转换酶(ACE)抑制剂、钙通道拮抗剂、血管紧张素受体拮抗剂和新型β受体阻滞剂(如卡维地洛)治疗自发性高血压大鼠(SHR),除了改善内皮依赖性松弛外,还可导致不同血管床小动脉结构改变的回归。一些高血压患者的研究表明,用一些ACE抑制剂(西拉普利和培哚普利)或缓释钙通道拮抗剂(硝苯地平)治疗在臀皮下活检获得的小动脉中产生类似的效果:在治疗下,结构和内皮依赖性松弛都得到改善。相比之下,高血压患者血压控制良好,但使用受体阻滞剂阿替洛尔治疗,在三项研究中均未显示出小动脉结构或内皮功能的任何改善。结论:尽管使用一些ACE抑制剂和缓释钙通道拮抗剂治疗至少一年可以纠正臀皮下小动脉的结构和内皮依赖性松弛,但这种明显的有益效果是否会导致高血压患者的发病率和死亡率降低仍有待确定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Vascular remodeling and endothelial function in hypertensive patients: effects of antihypertensive therapy.

Objective: To review studies of effects of antihypertensive agents on alterations in structure and function of small (resistance-size) arteries in hypertensive patients and in experimental hypertensive models, since these vessels may contribute to blood pressure elevation or to the complications of hypertension.

Main outcome measures: The structure and endothelium-dependent relaxation of small arteries obtained in hypertensive humans from gluteal subcutaneous biopsies, and from different vascular beds in hypertensive rats, without and after antihypertensive treatment, and studied on a wire-myograph or as pressurized arteries, are described as reported in different studies.

Results: Treatment of spontaneously hypertensive rats (SHR) with angiotensin converting enzyme (ACE) inhibitors, calcium channel antagonists, angiotensin receptor antagonists and novel beta blockers such as carvedilol, has been shown to result in regression of the altered structure of small arteries in different vascular beds, in addition to improved endothelium-dependent relaxation. Several studies in hypertensive patients have now shown that treatment with some ACE inhibitors (cilazapril and perindopril) or extended release calcium channel antagonists (nifedipine GITS) induces similar effects in small arteries obtained from gluteal subcutaneous biopsies: both structure and endothelium-dependent relaxation improve under treatment. In contrast, hypertensive patients with equally well-controlled blood pressure but treated with the beta blocker atenolol did not in any of three studies exhibit any improvement in the structure of small arteries or in endothelial function.

Conclusion: Although treatment for at least one year with some ACE inhibitors and extended release calcium channel antagonists corrects the structure and endothelium-dependent relaxation of gluteal subcutaneous small arteries, it still remains to be determined whether this apparently beneficial effect beyond blood pressure lowering of these and other agents with vascular protective properties will result in reduced morbidity and mortality in hypertensive patients.

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