a proteolytic enzyme synthesized, stored, and secreted by the juxtaglomerular
cells of the kidney; it plays a role in regulation of blood pressure by catalyzing the conversion of the plasma glycoprotein
angiotensinogen to
angiotensin I. This, in turn, is converted to
angiotensin II by an enzyme that is present in relatively high concentrations in the lung. Angiotensin II is one of the most potent
vasoconstrictors known, and also is a powerful stimulus of
aldosterone secretion.
Stimuli to the secretion of renin include sodium depletion, dehydration, serum albumin depletion, cirrhosis of the liver, cardiac failure, renal artery stenosis, and renal nerve stimulation.
Whenever blood flow to the kidney diminishes, renin is secreted and
angiotensin is formed. The angiotensin causes widespread
vasoconstriction and elevation of blood pressure consequent to greatly increased total peripheral resistance. A second effect, the increased secretion of
aldosterone, results in retention of salt and water by the kidneys and therefore increased extracellular fluid volume, cardiac output, and arterial pressure. Additionally, the angiotensin acts
directly on the kidneys to cause salt and water retention, which causes a long-term increase in arterial blood pressure.
renin-angiotensin-aldosterone system the regulation of sodium balance, fluid volume, and blood pressure by secretion of renin in response to reduced perfusion of the kidney. Renin hydrolyzes a plasma globulin to release
angiotensin I, which is rapidly hydrolyzed to angiotensin II, which in turn stimulates
aldosterone secretion. Aldosterone brings about sodium retention, water retention, increase in blood pressure, and restoration of renal perfusion, which shuts off the signal for renin release. Angiotensin II is a potent
vasoconstrictor, which also increases blood pressure.

The role of the renin-angiotensin-aldosterone system in regulation of blood pressure. Solid lines represent positive interactions; broken lines show negative interactions or feedback inhibition. From Cotran et al., 1994.