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在充血性心力衰竭病人,静脉和小动脉张力的代偿性增高常引起泵血功能的进一步恶化,引起这一血管收缩的因素包括交感神经活性增高,可能还有血管壁对加压刺激的反应性过高.在这些病人,肾素-血管紧张素系统也参与复杂的血管张力调节.充血性心力衰竭病人常不能排钠,也缺乏保持钠平衡的能力.血管紧张素Ⅱ是醛固酮分泌的主要刺激物,因而在理论上可以预期,阻断肾素-血管紧张素系统会在某种程度上逆转钠滞留.充血性心力衰竭时的肾素-血管紧张素系统
In patients with congestive heart failure, compensatory increases in venous and arteriolar tension often cause further deterioration in pump function. Factors that cause this vasoconstriction include increased sympathetic activity, and possibly the response of the vessel wall to pressurized stimuli In these patients, the renin-angiotensin system is also involved in complex vascular tone regimens, and patients with congestive heart failure often lack sodium or sodium supplementation.2 Angiotensin II is the major aldosterone secretion It is therefore theoretically expected that blocking the renin-angiotensin system would reverse sodium retention to some extent, and that the renin-angiotensin system in congestive heart failure