the enzyme system that forms and destroys the hormone hypertensin. It participates in the regulation of the level of arterial pressure, in the functioning of the kidneys, and in the water-salt metabolism of the body.

Renin is a proteolytic enzyme that acts on the angiotensinogen, or hypertensinogen, of the plasma and lymph to form a decapeptide—angiotensin I. The enzyme contained in the lungs and kidneys acts on angiotensin I and splits off its terminal dipeptide. Angiotensin I is then converted to active angiotensin II, also known as hypertensin or angiotonin. Angiotensin II constricts the blood vessels and stimulates the secretion of other hormones that influence vascular tone and the water-salt metabolism; these hormones include catecholamines, aldosterone, vasopressin, and prostaglandins. Angiotensin II also stimulates the contraction of the uterus.

Human arterial blood contains an average of 2.5 × 10^-6 mg of hypertensin per 100 milliliters of plasma. In venous blood the hypertensin concentration is much less because in the tissues it is bonded to receptors and destroyed by enzymes called angio-tensinases. The secretion and activity of renin, and consequently, also the concentration of hypertensin in the blood plasma, increase when the adrenal medulla or sympathetic nerves are excited, when there is a depletion of Na in the body or loss of blood, when blood circulation in the kidneys is disrupted, and during pregnancy. Excess Na in the body suppresses the activity of the renin-angiotensin system.

Activation of the renin-angiotensin system is one of the important factors in the development of both hypertonia, especially malignant hypertonia caused by kidney disease, and edemas, which occur with kidney disease and cardiac insufficiency. In cases of hypertonia caused by a tumor of the adrenal cortex, the activity of the renin-angiotensin system is low. The activity of renin and the concentration of hypertensin in the blood are determined by a diagnostic test performed on an individual exhibiting hypertonicity.