Chung O, Stoll M, Unger T
Department of Pharmacology, University of Kiel, Germany.
Blood Press Suppl. 1996;2:47-52.
The renin-angiotensin system (RAS) is an important factor in the pathogenesis of cardiovascular diseases, including hypertension and congestive heart failure. The RAS also contributes to media hypertrophy and neointima formation. The recent development of specific, highly selective, nonpeptide angiotensin II (A II)-receptor ligands/antagonists was the basis for the identification of the A II-receptor subtypes, AT1 and AT2, which display a heterogeneous distribution. Virtually all known physiologic actions of A II have been attributed to AT1 receptors; much less is known about AT2 receptors. Cell growth, proliferation, or both are mediated by AT1 receptors, whereas stimulation of AT2 receptors leads to an inhibition of cell proliferation and possibly induces cell differentiation. Under physiologic conditions. AT1 receptors may facilitate angiogenesis while AT2 receptors inhibit it. Under pathophysiologic conditions. AT2 receptors could be up-regulated to control excessive growth mediated in part by AT1 receptors. Characterization of the angiotensin-receptor subtypes has advanced our knowledge of the various functions of A II in the pathogenesis of hypertension and related diseases. It is hoped that eventually we will be able to develop even more specific blocking agents of the pathogenic effects of A II.
肾素-血管紧张素系统（RAS）是包括高血压和充血性心力衰竭在内的心血管疾病发病机制中的一个重要因素。RAS还与血管中层肥厚和内膜增生有关。特异性、高选择性、非肽类血管紧张素II（A II）受体配体/拮抗剂的最新进展是鉴定A II受体亚型AT1和AT2的基础，这两种受体表现出异质性分布。实际上，A II的所有已知生理作用都归因于AT1受体；而关于AT2受体的了解则少得多。细胞生长、增殖或两者均由AT1受体介导，而刺激AT2受体则导致细胞增殖受抑制，并可能诱导细胞分化。在生理条件下，AT1受体可能促进血管生成，而AT2受体则抑制血管生成。在病理生理条件下，AT2受体可能上调，以控制部分由AT1受体介导的过度生长。血管紧张素受体亚型的特征描述增进了我们对A II在高血压及相关疾病发病机制中各种功能的认识。希望最终我们能够开发出更具特异性的阻断A II致病作用的药物。
