In this foundational lecture, we will explore the contrasting roles of angiotensin-converting enzyme (ACE) and angiotensin-converting enzyme 2 (ACE2) in regulating inflammation and tissue homeostasis through the renin-angiotensin-aldosterone system (RAAS). We will analyze how ACE promotes proinflammatory effects via angiotensin II and its receptors, particularly AT1R, while ACE2 counters this activity through the generation of angiotensin-(1–7) and stimulation of MAS receptors. Emphasis will be placed on the downstream effects of receptor activation and the clinical relevance of this balance. This mechanistic understanding will prepare us for the following session on pharmacological agents—ACE inhibitors and ARBs—and their therapeutic implications in hypertension, cardiovascular disease, and inflammation. 

Learning Objectives:

1. Differentiate between the enzymatic functions of ACE and ACE2 in the RAAS pathway.

2. Identify the primary receptor targets of angiotensin II and angiotensin-(1–7), including AT1R, AT2R, and MAS receptor.  

3. Explain how activation of these receptors leads to either proinflammatory or anti-inflammatory outcomes. 

4. Illustrate the molecular and physiological consequences of the ACE/ACE2 axis imbalance in disease states.