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血管紧张素转换酶抑制的心脏保护机制。血管紧张素II-一氧化氮平衡。

Cardioprotective mechanisms of ACE inhibition. The angiotensin II-nitric oxide balance.

作者信息

Gibbons G H

机构信息

Molecular and Cellular Vascular Biology Research Laboratory, Brigham and Women's Hospital, Boston, Massachusetts, USA.

出版信息

Drugs. 1997;54 Suppl 5:1-11. doi: 10.2165/00003495-199700545-00003.

Abstract

The current challenge facing clinicians is to develop pharmacotherapies that move beyond the treatment of symptoms towards a new agenda in cardiovascular therapeutics that includes interventions to actually prevent the development of end-stage coronary heart disease. The development of new strategies to alter the natural history of cardiovascular disease will be fostered by gaining insights into the fundamental pathobiological mechanisms that promote the morbidity and mortality associated with these disorders. An emerging body of evidence indicates that locally generated vasoactive substances such as angiotensin II and nitric oxide are important determinants of the natural history of vascular disease. It is anticipated that ongoing clinical trials will extend the concept that modulating the activity of vasoactive substances generated by the endothelium has important implications for altering the course of coronary heart disease.

摘要

临床医生目前面临的挑战是开发药物疗法,使其超越症状治疗,迈向心血管治疗的新议程,其中包括采取干预措施切实预防终末期冠心病的发展。通过深入了解促进这些疾病相关发病和死亡的基本病理生物学机制,将推动改变心血管疾病自然史的新策略的发展。越来越多的证据表明,局部产生的血管活性物质,如血管紧张素II和一氧化氮,是血管疾病自然史的重要决定因素。预计正在进行的临床试验将扩展这样一个概念,即调节内皮产生的血管活性物质的活性对改变冠心病进程具有重要意义。

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