The RAAS system (Renin-Angiotensin-Aldosterone-System) centers on both blood volume and blood pressure - and as you are likely aware the two things are deeply intertwined.
Renin- [from the kidney] a renal protein with both endocrine and enzymatic functions. gets released systemically into the bloodstream and stimulates the conversion of angiotensinogen (-ogen --- tend to generate something else downstream) in this case, to angiotensin I. More on that later. Renin initiates the cascade of events below in two specific scenarios: a.) hypotension as sensed by the baroreceptors in the kidney and/or b.) reduced levels of sodium or sodium delivery to the distal tubules. Renin release is not just for isolated medical illness. Think of traumatic causes of volume depletion too - like hemorrhage or burns to name a few. From a medical standpoint though imagine how diseases with the kidneys or congestive heart failure can cause drastic dysregulations within this same system... that's where fluid balance and homeostasis can get quite complex. In renal disease this system increases the hemodynamic load unnecessarily including some toxins like creatinine.
Angiotensin- [from the lungs] if you break this term down angio means vessel, and tense for a lack of better terms means to constrict or tighten. This decreases the diameter inside of your vessels and increases peripheral resistance. You can imagine what this action would do for blood pressure regulation. Angiotensin comes in two forms I and II. Angiotensin I has no direct biological function however angiotensin converting enzymes (ACE) in the lungs convert this to the biologically active form Angiotensin II. Angiotensin II kick starts your adrenal glands and has them secrete aldosterone.
Aldosterone- [from the adrenal glands] this hormone that comes from the cortex of your adrenal glands helps to reabsorb both sodium (salt) and water while simultaneously excreting potassium and hydrogen. Remember where sodium goes, water typically follows. Reabsorption of water helps bulk up your intravascular volume which would in turn supports an improvement in venous return and therefore in systemic blood pressure. As a reminder arterial blood pressure is equal to the product of your cardiac output (affected by aldosterone directly) and total peripheral resistance (affected by angiotensin II directly).
As blood pressure and blood volume increase due to the actions of angiotensin II and aldosterone, this feedback reduces the initial stimuli that triggered renin release (like low blood pressure and sodium), thereby gradually restoring homeostasis. When our bodies natural negative feedback loops fail to work properly -- medications may be able to help!
When it comes to BP regulation, there may be times when we want the RAAS system to be put in check via other means. Hypertension is usually a result of RAAS overactivity. You may have heard of ACE inhibitor drugs in class (drugs ending in -opril like captopril, lisinopril protect the kidney and therefore reduce blood pressure. Their direct mechanism works against this RAAS system, specifically the angiotensin conversion piece. Additionally, another class of drugs called ARB's (angiotensin II receptor blockers halt this cascade further downstream and therefore have a different mechanism than ACE inhibitors. These drugs end in -artan, losartan and valsartan are some of the most common you may encounter in the field.
In closing, one of the most critical regulatory systems in the human body is the renin-angiotensin-aldosterone system (RAAS). Due to its vital function in systemic vasoconstriction, the renin-angiotensin-aldosterone system (RAAS) was the first neurohormonal system to be investigated in heart failure. The RAAS is a hormonal system that regulates blood pressure and fluid balance in the body and controls tissue perfusion by preserving the balance of arterial pressure. As we discussed, it is ubiquitous in multiple organ systems. We hope you enjoyed this review.
January 6, 2025
Author: Joshua Ishmael, MBA, MLS(ASCP)CM, NRP
Pass with PASS, LLC
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