Oliver J A
College of Physicians and Surgeons, Department of Medicine, Columbia University, New York, NY 10032.
Curr Opin Nephrol Hypertens. 1993 Mar;2(2):299-306. doi: 10.1097/00041552-199303000-00018.
The cellular and molecular mechanisms whereby hypertension causes vascular and cardiac disease are beginning to be understood. Angiotensin II, perhaps because so many probes to explore its action are available, is emerging as a central pathogenetic factor in the development of both vascular and cardiac hypertrophy. It is clear that this peptide has direct growth effects on vascular smooth muscle cells and cardiocytes as well as indirect effects by stimulating the synthesis of growth factors or potentiating their effects. However, the details of its action need clarification. Abnormalities in endothelium-derived relaxing factor regulation are a new pathogenetic mechanism of hypertension and are also likely to be intimately involved in the development of hypertensive cardiovascular disease. In the clinical arena, converting enzyme inhibitors are emerging as the best antihypertensive agents, and new therapeutic trials and further support to the suspicion that, when in doubt, it is better to treat.
高血压引发血管和心脏疾病的细胞及分子机制正逐渐被人们所了解。血管紧张素II或许是因为有众多可用于探究其作用的方法，正成为血管和心脏肥大发展过程中的核心致病因素。显然，这种肽对血管平滑肌细胞和心肌细胞具有直接的生长作用，同时还通过刺激生长因子的合成或增强其作用产生间接影响。然而，其作用的具体细节仍需阐明。内皮源性舒张因子调节异常是高血压的一种新致病机制，也可能与高血压性心血管疾病的发展密切相关。在临床领域，血管紧张素转换酶抑制剂正成为最佳的抗高血压药物，新的治疗试验进一步支持了一种怀疑，即在存在疑问时，治疗总归是更好的选择。
