Katz A M
Department of Medicine, University of Connecticut Health Center, Farmington 06030.
Heart Dis Stroke. 1992 May-Jun;1(3):151-4.
The actions of angiotensin II can be described in terms of the three paradigms listed in Table 1. According to the first paradigm (organ physiology), angiotensin II is a pressor, while the second (cell biochemistry) views it as an extracellular messenger that, by promoting Ca2+ release within cells, causes vasoconstriction and a weak positive inotropic response by the heart. However, neither of these paradigms fully explains the remarkable ability of angiotensin converting enzyme inhibitors to improve the prognosis for patients with heart failure. To account for these clinical effects of angiotensin converting enzyme inhibitors, we will probably need to invoke the third paradigm (gene expression), which views angiotensin II as a growth factor that promotes and modifies protein synthesis. Angiotensin II, therefore, should probably not be viewed simply as a vasoconstrictor with a side effect to promote hypertrophy, but instead as a growth factor that, because it utilizes Ca2+ to mediate its effects on gene expression, also increases smooth muscle tone and myocardial contractility. This view of angiotensin II as a growth factor helps us to understand the clinical benefit of angiotensin converting enzyme inhibitors as arising from inhibition of maladaptive changes in the failing heart (gene expression) as well as from the reduced afterload (organ physiology) that results from decreased smooth muscle tone (cell biochemistry).
血管紧张素II的作用可用表1中列出的三种范例来描述。根据第一种范例（器官生理学），血管紧张素II是一种升压物质，而第二种范例（细胞生物化学）则将其视为一种细胞外信使，它通过促进细胞内钙离子的释放，导致血管收缩以及心脏产生微弱的正性肌力反应。然而，这两种范例都无法完全解释血管紧张素转换酶抑制剂改善心力衰竭患者预后的显著能力。为了解释血管紧张素转换酶抑制剂的这些临床效果，我们可能需要引入第三种范例（基因表达），该范例将血管紧张素II视为一种促进和修饰蛋白质合成的生长因子。因此，血管紧张素II或许不应仅仅被视为一种具有促进肥大副作用的血管收缩剂，而应被看作是一种生长因子，由于它利用钙离子来介导其对基因表达的作用，所以也会增加平滑肌张力和心肌收缩力。将血管紧张素II视为生长因子的这种观点有助于我们理解血管紧张素转换酶抑制剂的临床益处，这种益处源于抑制衰竭心脏中的适应性不良变化（基因表达）以及平滑肌张力降低（细胞生物化学）所导致的后负荷降低（器官生理学）。
