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肾素-血管紧张素-醛固酮系统(R-A-A系统)是血压调节的三个主要生理调控机制之一。肾素选择性地切断血管紧张素原的Leu~(10)-Leu~(11)肽键,生成血管紧张素Ⅰ(AⅠ)。AⅠ在肺循环和小血管床被血管紧张素转换酶从C端脱下His-Leu-OH,生成具有强烈缩血管作用的八肽即血管紧张素Ⅱ(AⅡ)。AⅡ在血管紧张素转化酶A的作用下失去N端的门冬氨酸生成具有促醛固酮分泌作用的血管紧张素Ⅲ,同时也被酶逐渐降解失活。肾素是这一系列酶促反应的限速酶。抑制了肾素的活性就减少了AⅠ的生成,从而亦减少了AⅡ和AⅢ的生成,有利于降低因肾素过多而引起的高血压。
The renin-angiotensin-aldosterone system (R-A-A system) is one of the three major physiological regulators of blood pressure regulation. Renin selectively sequesters the Leu ~ (10) -Leu ~ (11) peptide bond of angiotensinogen to generate angiotensin Ⅰ (AⅠ). A Ⅰ His-Leu-OH was removed from the C-terminal by the angiotensin converting enzyme in the pulmonary circulation and small vessel wall to generate the octapeptide, angiotensin Ⅱ (AⅡ), which has a strong vasoconstrictor effect. A Ⅱ in the role of angiotensin converting enzyme A loss of N-terminal aspartate to produce the secretion of aldosterone-induced angiotensin Ⅲ, but also by the gradual degradation of enzyme inactivation. Renin is the rate-limiting enzyme in this series of enzymatic reactions. Inhibition of renin activity to reduce the generation of A Ⅰ, which also reduces the A Ⅱ and A Ⅲ generation, help to reduce hypertension caused by excessive renin.