Schiffrin E L
MRC Multidisciplinary Research Group on Hypertension, University of Montreal, Quebec, Canada.
Scand Cardiovasc J Suppl. 1998;47:15-21. doi: 10.1080/140174398428009.
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.
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.
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.
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.
回顾抗高血压药物对高血压患者及实验性高血压模型中小（阻力型）动脉结构和功能改变的影响研究，因为这些血管可能导致血压升高或高血压并发症。
描述了在接受和未接受抗高血压治疗的情况下，从高血压患者臀皮下活检以及高血压大鼠不同血管床获取的小动脉的结构和内皮依赖性舒张功能，这些小动脉在钢丝肌动描记器上或作为加压动脉进行研究，如不同研究所报道。
已表明，用血管紧张素转换酶（ACE）抑制剂、钙通道拮抗剂、血管紧张素受体拮抗剂以及新型β受体阻滞剂（如卡维地洛）治疗自发性高血压大鼠（SHR），除改善内皮依赖性舒张功能外，还可使不同血管床小动脉的结构改变恢复正常。目前多项针对高血压患者的研究表明，使用某些ACE抑制剂（西拉普利和培哚普利）或缓释钙通道拮抗剂（硝苯地平控释片）治疗，可使从臀皮下活检获取的小动脉产生类似效果：治疗后小动脉结构和内皮依赖性舒张功能均得到改善。相比之下，在三项研究中的任何一项里，血压控制同样良好但使用β受体阻滞剂阿替洛尔治疗的高血压患者，其小动脉结构或内皮功能均未出现任何改善。
尽管使用某些ACE抑制剂和缓释钙通道拮抗剂治疗至少一年可纠正臀皮下小动脉的结构和内皮依赖性舒张功能，但这些具有血管保护特性的药物除降低血压外的这种明显有益作用是否会降低高血压患者的发病率和死亡率，仍有待确定。
