The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system is a hormone system that helps regulate long-term blood pressure and blood volume in the body.

The system can be activated when there is a loss of blood volume or a drop in blood pressure (such as in a hemorrhage).

If the perfusion of the juxtaglomerular apparatus in the kidneys decreases, then the juxtaglomerular cells release the enzymatic hormone renin. Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries. Angiotensin I may have some minor activity, but angiotensin II is more potent.

Angiotensin II has a variety of effects on the body:

• It is a potent vasoconstrictor.
• In the kidneys, it constricts glomerular afferent arterioles. This decreases the glomerular filtration rate (GFR), which in turn raises systemic arterial blood pressure.
• It also acts on the adrenal cortex causing the release of aldosterone. Aldosterone acts on the tubules (i.e. the distal convoluted tubules and the cortical collecting ducts) in the kidneys, causing them to reabsorb more sodium and water from the urine. Aldosterone also acts on the central nervous system to increase a person's appetite for salt, and to make them feel thirsty.

These effects directly act to increase the amount of fluid in the blood, making up for a loss in volume, and to increase blood pressure.

The renin-angiotensin system is often manipulated clinically to treat high blood pressure. Inhibitors of angiotensin-converting enzyme are often used to reduce the formation of the more potent angiotensin II. Alternatively, angiotensin receptor blockers (ARBs) can be used to prevent angiotensin II from acting on angiotensin receptors.

Interestingly, ACE cleaves a number of other peptides, and in this capacity is an important regulator of the kinin-kallikrein system.