腎素-血管昇壓素-醛固酮系統(renin-angiotensin-aldosterone system, RAAS)是心血管、腎臟及腎上腺皮質功能之重要調節系統；而過度活化與心血管及腎臟疾病有直接的關連性。血管昇壓素轉換酵素抑制劑(angiotensin-converting enzyme inhibitors, ACEI)與血管昇壓素接受器阻斷劑(angiotensin-receptor antagonists, ARB)可藉由阻斷RAAS來降低高血壓和蛋白尿；然而卻使得血管昇壓素II(angiotensin II)於腎素分泌時之負回饋減少，而導致血清腎素活性(plasma renin activity, PRA) 與血清腎素濃度(plasma renin concentration, PRC)增加；過去的研究指出PRA升高與器官的損害有關，如左心室肥大及腎功能不良，可能影響此類藥物原有之阻斷效果。Aliskiren為目前唯一之腎素抑制劑(direct rennin inhibitors, DRI)，藉由阻斷腎素的活性來達到降血壓及降蛋白尿的效果。Aliskiren可有效降低PRA，但PRC仍會升高。藉由更有效地抑制RAAS，aliskiren對高血壓合併有糖尿病腎病變患者有腎臟保護效果；在心臟方面，也具減少左心室肥大與治療心衰竭之效果。
 

The renin-angiotensin-aldosterone-system (RAAS) is the main regulatory system of cardiovascular, renal, and adrenal function. However, over-activation of RAAS may induce cardiovascular and renal damage. Hypertension and proteinuria can be precisely reduced by angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB). Both ACEI and ARB block the RAAS and increase plasma renin activity (PRA) and plasma renin concentration (PRC) by negative feedback of angiotension II inhibition. Both of PRC and PRA had been elevated to associate with end-organ damage, such as left ventricular hypertrophy and renal dysfunction. Aliskiren is the only one direct rennin inhibitor (DRI) that blocks the active site of renin to reduce blood pressure and proteinuria. Even aliskiren has been lower PRA effectively, but PRC remains high. Aliskiren has renal protection in hypertension combined diabetic nephropathy patient. In addition, it decreases left ventricular hypertrophy and treats for heart failure in cardiovascular effect.