The release of aldosterone from the adrenal cortex is stimulated by the formation of angiotensin II. 

Aldosterone's Role in the Renin-Angiotensin-Aldosterone System

The renin-angiotensin system (RAS) is also referred as the renin-angiotensin-aldosterone system (RAAS) due to the role of the hormone aldosterone within this system. Aldosterone is released from the adrenal cortex when angiotensin is formed. As a result, this hormone can interrupt the homeostasis of this endocrine system. 

Grand Valley State University

The renin–angiotensin system (RAS) plays a central role in cardiovascular physiology by maintaining blood pressure, controlling blood volume, regulating sodium concentration in the plasma, and keeping the electrolytes balanced.  When homeostasis is perturbed, the RAS can cause inflammation and structural remodeling of the tissue.  This can lead to vascular, renal, and cardiac damage.

Renin–Angiotensin System (RAS)

Vaduganathan, M., Vardeny, O., Michel, T., McMurray, J., Pfeffer, M., &amp; Solomon, S. (2020). Renin–Angiotensin–Aldosterone System Inhibitors in Covid-19. New England Journal of Medicine, 382(24). doi:10.1056/nejmc2013707.
https://www.nejm.org/doi/full/10.1056/NEJMsr2005760

Renin–Angiotensin–Aldosterone System Inhibitors in Patients with Covid-19

Rüster, C., & Wolf, G. (2006). Renin-Angiotensin-Aldosterone System and Progression of Renal Disease. Journal of the American Society of Nephrology, 17(11), 2985-2991. doi:10.1681/asn.2006040356.


Renin-Angiotensin-Aldosterone System and Progression of Renal Disease

Physiological Components of the RAS

Ang II is a hormone that is regulated by the RAS.  The excessive adipose tissue associated with obesity is known to secrete this molecule which stimulates inflammation, insulin resistance, oxidative stress, and vasoconstriction.  Insulin resistance can exacerbate these conditions by further stimulating the RAS.  A relationship exists between pancreatic beta islet cells (B-cells) and the RAS: B-cell dysfunction leads to increased expression AT1R, the receptor for Ang II, and insulin resistance while RAS inhibition increases B-cell function and insulin sensitivity.  

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