Unraveling the complex pathophysiology of heart failure: insights into the role of renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS)

Abstract

Heart failure (HF) is a widespread disease with significantly elevated mortality, morbidity, and hospitalization rates. Dysregulation of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) are both postulated to be significant regulators of cardiovascular function, thereby playing a pivotal role in its pathophysiology. The RAAS is a sophisticated hormonal system that controls electrolyte homeostasis, fluid balance, and blood pressure. Angiotensin II, which operates to constrict blood vessels and raise blood pressure, is its principal effector molecule. The RAAS is frequently hyperactive in HF, which increases fluid retention and worsens cardiac function. The SNS is frequently hyperactive in heart failure, which increases the workload on the heart and worsens symptoms. This review will discuss what is currently known about the pathophysiology of heart failure, specifically in the context of RAAS and the SNS, in-depth to emphasize the knowledge gap that necessitates more research.

Keywords: Angiotensin II; Heart failure; Renin-angiotensin-aldosterone system.