Figure 3.

Schematic diagram of the renin–angiotensin–aldosterone system (RAAS), the kinin–kallikrein system and the anti-hypertensive effect of ACE. The protein angiotensinogen is formed in the liver and renin aspartic protease protein causes the breakdown of angiotensinogen into the decapeptide angiotensin I. Through the cleaving action of ACE-1, angiotensin I is converted into angiotensin II, whose action recruits the second messenger 1,4,5-inositol trisphosphate (IP³), resulting in the formation of calcium ions (Ca²⁺), leading to an increase in blood pressure through vasoconstriction. In the adrenal cortex, the secretion of angiotensin II enhances the production of aldosterone that causes the formation of extracellular fluid, thereby increasing blood pressure. Bradykinin a peptide produced through enzyme action of kallikrein, it is inactivated by ACE-1 and enhances the release of calcium ions [223]. Immune-regulating lipids and prostaglandins signal the opening of arteries in the heart through vasodilation, alleviating blood pressure [224].