Unterberg C, Kreuzer H, Buchwald A B
Abteilung Kardiologie und Pulmonologie der Medizinischen Universitätsklinik Göttingen.
Med Klin (Munich). 1998 Jul 15;93(7):416-25. doi: 10.1007/BF03042638.
The renin-angiotensin system is mainly involved in several cardiovascular diseases and in the pathophysiology of heart failure. It exists as a circulating and a local system which can be differently regulated. Interventions in this system by angiotensin-converting enzyme (ACE) antagonists or angiotensin-receptor antagonists slow the progression of heart failure and result in prolongation of life expectancy and improvement of hemodynamics.
The main underlying mechanisms are: 1. Heart failure results in activation of the renin-angiotensin system as a compensatory mechanism with elevation of circulating angiotensin II, norepinephrine and vasopressin. Antagonists of this compensatory mechanisms acutely result in improvement of the hemodynamic situation. 2. Elevated circulating and local renin-angiotensin systems cause chronic structural myocardial and vascular effects. Angiotensin-converting enzyme antagonists and angiotensin-receptor blockers modulate and partly antagonize these structural changes such as myocardial hypertrophy, myocardial fibrosis and vascular proliferative responses. Gene and receptor regulation of the system are currently not fully understood and are subject of intensive research. 3. The renin-angiotensin system is closely related to the bradykinin system and thus indirectly to nitric oxide and endothelial function. Bradykinin has multiple other effects on the hemostatic system as a well as on the myocardium and vascular system.
These complex interactions require further evaluation. Research with specific bradykinin antagonists will give new insights into this system.
肾素-血管紧张素系统主要参与多种心血管疾病及心力衰竭的病理生理过程。它以循环系统和局部系统的形式存在，且二者受到的调节有所不同。通过血管紧张素转换酶（ACE）拮抗剂或血管紧张素受体拮抗剂对该系统进行干预，可减缓心力衰竭的进展，延长预期寿命并改善血流动力学。
主要潜在机制如下：1. 心力衰竭会激活肾素-血管紧张素系统，作为一种代偿机制，导致循环中的血管紧张素II、去甲肾上腺素和血管加压素升高。对这种代偿机制的拮抗剂可急性改善血流动力学状况。2. 循环和局部肾素-血管紧张素系统的升高会导致慢性心肌和血管结构改变。血管紧张素转换酶拮抗剂和血管紧张素受体阻滞剂可调节并部分拮抗这些结构变化，如心肌肥大、心肌纤维化和血管增殖反应。目前对该系统的基因和受体调节尚未完全了解，仍是深入研究的课题。3. 肾素-血管紧张素系统与缓激肽系统密切相关，因此间接与一氧化氮和内皮功能相关。缓激肽对止血系统以及心肌和血管系统还有多种其他作用。
这些复杂的相互作用需要进一步评估。使用特定缓激肽拮抗剂的研究将为该系统带来新的见解。
