The RAAS Pathway: A Key Concept in Nursing
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This lesson covers the renin angiotensin aldosterone system, also known as the RAAS pathway. When you know this system, you have foundation knowledge that will help you understand several key concepts – endocrine function, fluid balance, hypertension treatment, heart failure treatment, and three classes of medications. As I discuss in my free class “How to Thrive in Nursing School Without it Taking Over Your Life,” this is a great example of how memorizing one fact can help you understand multiple important concepts.
The role of RAAS in the body
RAAS has two functions in the body – it helps maintain appropriate volume and it regulates systemic vascular resistance (SVR). Systemic vascular resistance (also known as total peripheral resistance) is the amount of force the vasculature exerts on circulating blood. There are three things which determine SVR: the length of the vasculature, the viscosity of the blood, and vessel diameter. Of these, the most variable is vessel diameter. So, when vessels constrict, SVR goes up and when vessels dilate, SVR goes down. Both volume and SVR play a role in cardiac output, which contributes to blood pressure. So, in a nutshell, RAAS functions as an important component of blood pressure regulation.
The three components of RAAS
The three components of RAAS are renin, angiotensin and aldosterone.
- Renin is an enzyme. Remember, enzymes are biological catalysts that increase the rate of metabolic physiological processes and make things happen. Renin is released by the JG cells of the kidneys when blood pressure and renal perfusion are low.
- Angiotensin is a hormone. Recall that hormones are molecules that are produced in one part of the body, but trigger a specific reaction in a target tissue or target organ in another distant part of the body. And, of course, hormones can be either excitatory or inhibitory. There are multiple forms of angiotensin, and the one responsible for the effects of the RAAS pathway is angiotensin II.
- Aldosterone is also a hormone. It is created from cholesterol and produced in the adrenal cortex. It helps regulate salt and water balance in the body.
The RAAS pathway
The renin-angiotensin-aldosterone system is activated by three different mechanisms: detection of decreased renal perfusion pressure, detection of low sodium levels, and through activation of the SNS. Let’s go through the RAAS pathway step-by-step:
- Renin is released by the JG cells of the kidneys.
- Renin converts angiotensinogen (a protein produced in the liver) into angiotensin I.
- Angiotensin I passes through the vasculature of the pulmonary system and is activated by ACE (angiotensin converting enzyme).
- ACE turns angiotensin I into angiotensin II.
- Angiotensin II has a lot of jobs. It increases SVR through vasoconstriction, stimulates the reabsorption of sodium at the renal tubules, and stimulates the pituitary to release antidiuretic hormone. It also increases thirst to encourage fluid consumption. In addition, angiotensin II facilitates the release of norepinephrine, which is another potent vasoconstrictor, and tells the adrenal cortex to release aldosterone. It also stimulates cardiac hypertrophy, which comes into play in cardiac disorders such as chronic hypertension, myocardial infarction and heart failure.
- Aldosterone stimulates the kidneys to increase sodium and fluid retention.
All of these actions together achieve two things – increased fluid volume and vasoconstriction. With increased fluid volume, we have greater preload, higher cardiac output and higher blood pressure. Vasoconstriction increases SVR, which also increases blood pressure. So, the end result of RAAS activation is higher blood pressure.
Hypertension and RAAS
Medications that disrupt the RAAS pathway are commonly used in the treatment of hypertension. There are three classes of medications that achieve this goal: ACE inhibitors, angiotensin receptor blockers (ARBs), and aldosterone receptor blockers.
- ACE inhibitors such as lisinopril disrupt angiotensin converting enzyme (ACE) from converting angiotensin I into angiotensin II. Since angiotensin I is an inactive precursor, it doesn’t have an effect on blood pressure.
- ARBs disrupt the pathway by blocking angiotensin altogether. An example is losartan.
- Aldosterone receptor blockers such as spironolactone disrupt the pathway by blocking aldosterone and preventing the body from holding on to salt and water. The result is less fluid retention.
Hypotension and RAAS
We can also enhance the RAAS pathway to increase blood pressure with the medication giapreza, which is a pharmacological angiotensin II. Giapreza enhances the pathway to increase blood pressure in severely hypotensive patients in septic shock.
Heart failure and RAAS
Medications that disrupt the RAAS pathway are also used to treat patients with heart failure. Sustained activation of the renin-angiotensin-aldosterone system can contribute to and worsen heart failure due to vasoconstriction, fluid retention, and cardiac remodeling (changes in the heart’s structure and size). By disrupting the effects of angiotensin and aldosterone, patients with heart failure have less disease progression and improved quality of life.
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References:
Patel, P., Sanghavi, D. K., Morris, D. L., & Kahwaji, C. I. (2025). Angiotensin II. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK499912/
ScienceDirect. (n.d.). Angiotensin I. ScienceDirect. https://www.sciencedirect.com/topics/neuroscience/angiotensin-i
Scott, J. H., Menouar, M. A., & Dunn, R. J. (2025). Physiology, Aldosterone. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK470339/
Trammel, J. E., & Sapra, A. (2025). Physiology, Systemic Vascular Resistance. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK556075/
Trerattanavong, K., & Chen, J. (Steven). (2025). Biochemistry, Renin. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK556056/
Last Updated on August 8, 2025 by Maureen Osuna, MSN, RN