Angiotensin

Angiotensinogen, angiotensin I and angiotensin II are peptides involved in maintanence of blood volume and pressure. They play an important role in the renin-angiotensin system.

Table of contents

1 Angiotensinogen
2 Angiotensin I
3 Angiotensin II

Angiotensinogen

Angiotensinogen is the precursor molecule, and it is produced mainly in the liver, (although other sites have been thought to contribute to local effects of the molecule).

Production of the peptide is increased by corticosteroids, oestrogens, thyroid homones, and notably, angiotensin II.

In humans, the peptide sequence for angiotensinogen (485 amino acids long) which contains (immediatly after the signal peptide) the 10 amino acid:

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu

When blood pressure decreases in the kidneys, they produce an enzyme called renin. Renin acts to cleave the peptide bond between the leucine (Leu) and the valine (Val) residues. The ten amino acid peptide (bold) angiotensin I is created.

Angiotensin I

Angiotensin I has little biological effect. Its main role is to become angiotensin II.

Angiotensin I is a ten peptide chain. When the last two amino acids are removed, it becomes angiotensin II.

Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu

The enzyme that cleaves this precursor is called angiotensin converting enzyme (ACE). This enzyme is a target for drugs (ACE inhibitors) that inactivate it, decreasing the rate of angiotensin II production.

Angiotensin II

This eight amino acid long molecule has a number of effects throughout the body.

It is a potent vasocontrictor, causing arteries and veins to constrict. The constriction of these vessels will push up blood pressure.

Angiotensin II also acts on the brain to increase the sense of thirst, and increase the desire for salt. It also increases the secretion of vasopressin and ACTH.

It acts on the adrenal cortex, causing it to produce aldosterone, a chemical that causes the kidneys to retain sodium, and lose potassium. As well as this, it is thought to directly work on the kidneys to increase sodium resorption at the proximal tubules.

It has been thought that angiotensin II could be a cause of cardiac muscle hypertrophy (when the heart wall grows bigger).

Angiotensin II is destroyed by angiotensinases that are located in the vascular beds of most tissues.