Holmer S R, Schunkert H
Klinik und Poliklinik für Innere Medizin II, Universität Regensburg, Germany.
Basic Res Cardiol. 1996;91 Suppl 2:65-71. doi: 10.1007/BF00795365.
The risk to suffer from cardiovascular events may be modulated, in part, by neurohormonal systems. Neurohormones such as angiotensin II or aldosterone may be activated secondary to congestive heart failure or in the course of an acute myocardial infarction. These systems, if activated, will subject the failing heart to increased hemodynamic load and, thus, further compromise cardiac function. In addition, structural changes of the heart and vessels occurring with pressure or volume overload may be amplified by the growth promoting effects of these agents. Taken together, the interaction of underlying cardiovascular disease and activated neurohormones may often determine clinical symptoms and prognosis. More recently, growing evidence suggests that the basal, genetically determined, activity of the renin angiotensin aldosterone system may relate to the development of cardiovascular disease as well. In particular, variants of the angiotensinogen and angiotensin converting enzyme genes have been associated with essential hypertension, myocardial infarction, or left ventricular hypertrophy. In this regard, the data suggest that the renin angiotensin aldosterone system may be one of the primary causes, rather than only a secondary co-factor, in the pathogenesis of these most important cardiovascular disorders. In light of the various options of pharmacological intervention, it seems important that ongoing clinical and molecular-genetic research will further define the role of the renin angiotensin system in clinical conditions or genetic risk profiles.
患心血管事件的风险可能部分受到神经激素系统的调节。诸如血管紧张素II或醛固酮等神经激素可能继发于充血性心力衰竭或在急性心肌梗死过程中被激活。如果这些系统被激活，将使衰竭的心脏承受增加的血流动力学负荷，从而进一步损害心脏功能。此外，压力或容量超负荷导致的心脏和血管结构变化可能会因这些因子的促生长作用而加剧。综上所述，潜在的心血管疾病与激活的神经激素之间的相互作用往往决定临床症状和预后。最近，越来越多的证据表明，肾素血管紧张素醛固酮系统的基础遗传决定活性也可能与心血管疾病的发生有关。特别是，血管紧张素原和血管紧张素转换酶基因的变异与原发性高血压、心肌梗死或左心室肥厚有关。在这方面，数据表明肾素血管紧张素醛固酮系统可能是这些最重要的心血管疾病发病机制中的主要原因之一，而不仅仅是一个次要的协同因素。鉴于药理学干预的各种选择，正在进行的临床和分子遗传学研究进一步明确肾素血管紧张素系统在临床情况或遗传风险概况中的作用似乎很重要。
