Renal injury is a common complication of primary hypertension.[1] Renin-angiotensin-aldosterone system (RAAS), including local and circulating RAAS, plays important roles in the blood pressure regulation and the pathogenesis of chronic renal injury.[2] Juxtaglomerular cells could secrete rennin, and then activate the angiotensinogen and lead to generation of angiotensin-I (AT-I).[3] In pulmonary vascular endothelial cells, AT-I was transmitted to angiotensin-II (AT-II) by angiotoninase (ACE). Here, ACE is linked to essential hypertension.