Morgan T, Brunner H R
Department of Physiology, University of Melbourne, Parkville, Australia.
Heart. 1996 Nov;76(3 Suppl 3):98-103. doi: 10.1136/hrt.76.3_suppl_3.98.
Renin-angiotensin is both a circulatory and a local tissue system. However, in most circumstances, renin present in the heart and blood vessels is taken up from the plasma, and the kidney is the prime source of this renin. Tissues can then modulate and control the production of angiotensin II. In various organs, angiotensin II has local actions. In the heart, working through the AT1 receptor, it increases contractility and may cause cardiocyte hypertrophy. Indirectly, the heart is also very much affected by the vascular actions of angiotensin II. However, the net result on the heart is the product of an important interaction between a large number of factors. There is little doubt that an inappropriately high plasma (and tissue) level of renin, related to sodium balance, is associated with increased left ventricular hypertrophy and cardiovascular complications. The genetic approach will lead to an understanding of genomic risk factors in hypertension and may identify control systems--at present unknown--which will lead to a new approach to the prevention of cardiovascular death. It is, however, unlikely that such a factor will clearly predict an individual's prognosis, but it will, rather, identify groups at risk. Constellations of genomic interactions with multiple environment factors reduce this power. Modification of the response to angiotensin II using present treatment, or interrupting the response at more distal sites, may enable us to achieve the beneficial effects on cardiac hypertrophy without the detrimental effects.
肾素-血管紧张素既是一种循环系统，也是一种局部组织系统。然而，在大多数情况下，心脏和血管中的肾素是从血浆中摄取的，而肾脏是这种肾素的主要来源。组织随后可以调节和控制血管紧张素II的产生。在各种器官中，血管紧张素II具有局部作用。在心脏中，通过AT1受体起作用，它可增加心肌收缩力并可能导致心肌细胞肥大。间接而言，心脏也会受到血管紧张素II血管作用的很大影响。然而，对心脏的最终影响是大量因素之间重要相互作用的结果。毫无疑问，与钠平衡相关的肾素血浆（和组织）水平过高会导致左心室肥厚和心血管并发症增加。遗传学方法将有助于了解高血压中的基因组危险因素，并可能识别目前未知的控制系统，这将带来预防心血管死亡的新方法。然而，这样一个因素不太可能明确预测个体的预后，而是会识别出有风险的群体。基因组与多种环境因素的相互作用组合会降低这种预测能力。使用现有治疗方法改变对血管紧张素II的反应，或在更远端部位阻断反应，可能使我们在不产生有害影响的情况下实现对心肌肥厚的有益作用。
