renin–angiotensin–aldosterone system
The renin–angiotensin–aldosterone system, or RAAS, is the body's master control for blood pressure and fluid balance, working like a thermostat that senses when pressure drops and acts to push it back up. When the kidneys sense low blood flow, they kick off a cascade of hormones that tightens vessels and tells the body to hold onto salt and water, raising the pressure back toward normal.
The cascade runs in steps. The kidney releases renin, an enzyme that converts angiotensinogen (from the liver) into angiotensin I. Angiotensin-converting enzyme, mostly in the lungs, then converts angiotensin I into angiotensin II, the system's powerful actor: it constricts blood vessels and stimulates the adrenal gland to release aldosterone, a hormone that makes the kidney retain sodium and water while excreting potassium. The net effect is higher blood volume and pressure.
This single pathway is the target of several major drug classes, which is why understanding it unlocks so much of cardiovascular pharmacology. ACE inhibitors block the angiotensin-converting step; angiotensin receptor blockers block angiotensin II at its receptor; aldosterone antagonists like spironolactone block the final hormone; and direct renin inhibitors block the first step. When the system is chronically overactive, as in heart failure and hypertension, calming it both lowers pressure and protects the heart and kidneys over time.
In chronic heart failure the RAAS is persistently switched on, so blocking it with an ACE inhibitor or angiotensin receptor blocker plus an aldosterone antagonist is a cornerstone of treatment.
A single overactive hormone system is targeted at multiple points to treat heart failure.
Because so many drugs converge on this one system, combining two RAAS-blocking drugs is usually avoided: it adds little extra benefit but markedly raises the risk of high potassium and kidney injury.