In this foundational pharmacology lecture, we explore how Angiotensin II (Ang II) contributes to cardiovascular hypertrophy and pathological remodeling, with a focus on the cellular mechanisms, extracellular matrix alterations, and hemodynamic effects. Based on Goodman & Gilman's authoritative text, this lecture outlines how Ang II directly impacts cardiac myocytes, vascular smooth muscle cells, and fibroblasts, and how it indirectly promotes remodeling through aldosterone and mineralocorticoid receptor activation.

We also contrast physiological versus pathological hypertrophy, highlighting the clinical implications of chronic Ang II signaling and the partial role of mineralocorticoid receptor antagonists in mitigating disease progression.

Ideal for students and practitioners revisiting cardiovascular pharmacology or learning it for the first time.

Objective:

• By the end of this talk, participants will be able to:
• Identify the key cardiovascular cell types affected by Angiotensin II.
• Describe how Ang II induces cardiac myocyte hypertrophy and promotes vascular smooth muscle cell proliferation and ECM production.
• Explain the role of aldosterone and mineralocorticoid receptor activation in extracellular matrix remodeling.
• Differentiate between the direct cellular effects and hemodynamic effects of Ang II on cardiovascular structure.
• Discuss why pathological remodeling induced by Ang II increases cardiovascular morbidity and mortality, and how pharmacologic interventions can help mitigate this process.
• Contrast pathological (e.g., pressure overload) and physiological (e.g., exercise-induced) cardiac hypertrophy in terms of sarcomere arrangement, capillary density, and reversibility.