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Role Of RAAS In Heart Failure And Side Effects Discussion Chapter

RAAS

The RAAS helps in regulating blood pressure and fluid balance. In heart failure, the reduced cardiac output and systemic blood pressure stimulate the RAAS as a compensatory mechanism, which in turn leads to increased retention of sodium and water, vasoconstriction, and elevated blood pressure. This activation of the RAAS is at first adaptive, but it basically contributes to the progression of heart failure and exacerbates atherosclerosis by promoting endothelial dysfunction, inflammation, and vascular remodeling.

It works this way: in response to heart failure, the RAAS system is activated as a compensatory mechanism (Pugliese et al., 2020). The process begins when the kidneys, sensing reduced blood flow and pressure, release the enzyme renin into the bloodstream. Renin converts angiotensinogen, a liver-produced protein, into angiotensin I, which is then converted into angiotensin II by angiotensin-converting enzyme (ACE) primarily in the lungs. Angiotensin II is a potent vasoconstrictor, which increases blood pressure by narrowing blood vessels (Senatore et al., 2021). Additionally, it stimulates the secretion of aldosterone from the adrenal glands, leading to sodium and water retention by the kidneys, thereby increasing blood volume...

Chronic vasoconstriction and fluid retention elevate...
…and atherosclerosis has led to the development of therapeutic strategies aimed at inhibiting this system to improve outcomes in patients with cardiovascular diseases. Medications such as ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) target different components of the RAAS, offering benefits such as reduced blood pressure, decreased risk of atherosclerotic events, and mitigation of heart failure progression.

Overall, the RAAS is important in the body's initial response to heart failure, but its chronic activation contributes significantly to the pathology of heart failure and atherosclerosis through mechanisms such as endothelial dysfunction, inflammation, and vascular remodeling. Targeting the RAAS therapeutically has become a cornerstone in managing these conditions, which shows the…

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References

Laranjo, L., Lanas, F., Sun, M. C., Chen, D. A., Hynes, L., Imran, T. F., ... & Chow, C. K.

(2024). World Heart Federation Roadmap for Secondary Prevention of Cardiovascular Disease: 2023 Update. Global Heart, 19(1). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10809857/

Pugliese, N. R., Masi, S., & Taddei, S. (2020). The renin-angiotensin-aldosterone system: acrossroad from arterial hypertension to heart failure. Heart Failure Reviews, 25, 31-42.

Romero-González, G., Rodríguez-Chitiva, N., Cañameras, C., Paúl-Martínez, J., Urrutia-Jou, M.,Troya, M., ... & Bover, J. (2024). Albuminuria, Forgotten No More: Underlining the Emerging Role in CardioRenal Crosstalk. Journal of Clinical Medicine, 13(3), 777. https://doi.org/10.3390/jcm13030777

Senatore, F., Balakumar, P., & Jagadeesh, G. (2021). Dysregulation of the renin-angiotensinsystem in septic shock: mechanistic insights and application of angiotensin II in clinical management. Pharmacological Research, 174, 105916.

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