- OMIM: 106150
- UniProt: P01019
- MGI: 87963
Angiotensin II is a scoring of the tissue hormones peptide hormone consisting of eight amino acids ( octapeptide ). It takes the key position in the responsible for the maintenance of blood pressure and water balance renin -angiotensin -aldosterone system (RAAS ).
The primary structure of angiotensin II, consisting of eight amino acids ( H2N -Asp -Arg -Val -Tyr -Ile- His-Pro -Phe- COOH) with a molecular mass of 1046.19 Da.
Angiotensin II is cleaved from the decapeptide angiotensin I in the body by the enzyme angiotensin converting enzyme (ACE). Angiotensin converting enzyme is the point of action of ACE inhibitors. Angiotensin I is formed by enzymatic cleavage of angiotensinogen by renin. The primary stimulus of renin release (and thus ultimately to the formation of angiotensin II) is a low blood pressure in the kidneys.
Mechanism of Action
The angiotensin II formed interacts with angiotensin receptors ( AT receptors ). By activation of the AT1 receptor in blood vessels can be primary contraction take place. In the kidney glomerular filtration rate is maintained as constant as possible by means of a constriction of the efferent blood vessels. In the adrenal angiotensin II stimulates aldosterone and epinephrine release and pituitary release of vasopressin. And the thirst is attributed to an acute stimulation of AT1 receptors in the hypothalamus. Chronic stimulation of the AT1 receptor on the other hand leads to a stimulation of mitogenic effects, and thus, for example, hypertrophy of the heart. Acute and chronic effects of angiotensin II on the AT1 receptor may indirectly by ACE inhibitors and directly by AT1 receptor antagonists ( sartans ) or saralasin be suppressed.
Angiotensin II also shows a high affinity to the AT2 receptor. The role of these receptors to the effects mediated by angiotensin II, however, is controversial. Animal experiments on mice gave evidence that the effect of AT2 receptors in the sense of counteraction has dampen the effects of AT1 receptors.
Angiotensinamid, a descendant of angiotensin II, is a kardiostimulierender and blood pressure- enhancing drug.
Angiotensin II is degraded by aminopeptidases in a multi-step process to produce inactive products. However Incidental intermediates such as angiotensin III and angiotensin IV may well still have a biological activity. Angiotensin III binds with moderate potency at the AT1 receptor, whereas angiotensin IV is a ligand to the still little explored AT4 receptor.
An alternative cleavage pathway of angiotensin II with the angiotensin-converting enzyme type 2 was only recently discovered.
Angiotensin, originally called Angiotonin or hypertensin was first described in 1940 by IH Page. He noted that the angiotensinogen formed in the liver is a substrate for the kidney enzyme renin that were found. As a result of an enzymatic reaction, a substance could be found which leads to vasoconstriction and an increase in blood pressure. But it still needed more than a decade until by Leonard T. Skeggs has been shown that angiotensin is a mixture of at least two different substances: the largely inactive angiotensin I and angiotensin II vascular twitch