Renin–angiotensin–aldosterone system

The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS) is a hormone system that is involved in the regulation of the plasma sodium concentration and arterial blood pressure.

When the plasma sodium concentration is lower than normal or the renal blood flow is reduced, the juxtaglomerular cells in the kidneys convert prorenin (an intracellular protein) into renin, which is then secreted directly into the circulation. Plasma renin then cuts a short, 10 amino acid long, peptide off a plasma protein known as angiotensinogen. The short peptide is known as angiotensin I. Angiotensin I is then converted, by the removal of 2 amino acids, to form an octapeptide known as angiotensin II, by the enzyme angiotensin-converting enzyme (ACE) found in the endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys. Angiotensin II is a potent vaso-active peptide that causes arterioles to constrict, resulting in increased arterial blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubular epithelial cells of the kidneys to increase the reabsorption of sodium ions from the tubular fluid back into the blood, while at the same time causing them to excrete potassium ions into the tubular fluid which will become urine.

If the RAAS is abnormally active, blood pressure will be too high. There are many drugs that interrupt different steps in this system to lower blood pressure. These drugs are one of the primary ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes.

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