Figure 2.

Schematic representation of the renin–angiotensin–aldosterone system (RAAS) and the hypertensive effect of angiotensin-I-converting enzyme (ACE-I). Angiotensinogen is converted to the decapeptide angiotensin-I by renin. ACE-I cleaves the C-terminal dipeptide His-Leu of angiotensin-I to form angiotensin-II. Binding of angiotensin-II to its receptor (AT1) stimulates the secretion of inositol 1,4,5-triphosphate (IP3) and aldosterone, which induce arteriolar vasoconstriction and increased intravascular fluid volume, respectively, resulting in increased blood pressure. Within the kallikrein–kinin system, kallikrein converts kininogen to bradykinin, which induces arteriolar vasodilation by prostaglandin secretion and binding of bradykinin with its receptor, resulting in decreased blood pressure. However, the hypotensive effect of bradykinin is largely dependent on the rate of degradation by ACE-I, which hydrolyzes bradykinin to form inactive metabolites.