Angiotensin 2 is an endogenous hormone which belongs to the class of so-called peptide hormones. Peptide hormones (synonym: proteohormones) are built up from the smallest individual components, the amino acids, and are water-soluble (hydrophilic/lipophobic). Angiotensin 2 itself consists of a total of eight amino acids.
Due to its water-soluble property, angiotensin 2 is not able to pass through the cell membrane independently and carry out its messenger function inside the cell. Therefore, its effect as a hormone can only unfold after binding to a suitable surface receptor. As part of the renin-angiotensin-aldosterone system (RAAS), angiotensin 2 plays a decisive role in the regulation of the water balance and the maintenance of blood pressure.
The formation and release of angiotensin 2 does not occur in the organism in arbitrary quantities. Rather, the tissue hormone angiotensin 2 is part of a specific activation cascade, the so-called renin-angiotensin-aldosterone system. In the course of this system, the kidney reacts to falling blood pressure or reduced blood circulation by releasing the enzyme renin.
An acute loss of common salt and water, which can be equated to a reduction in blood volume, also triggers a release of renin. As an enzyme, renin is able to split off the precursor of angiotensin 2, namely angiotensin 1, from the angiotensinogen formed in the liver cells. The conversion of the hormone precursor to the active hormone then takes place with the help of the angiotensin converting enzyme (ACE).
The surface receptor (AT-receptor) specific for the tissue hormone angiotensin 2 is mainly located on the outer side of the cell membrane of blood vessel, kidney and adrenal cells. By binding to the angiotensin 2 receptor of the blood vessels, a signalling chain is activated inside the smooth muscle cells, which triggers their contraction. In this way, the previously dropped blood pressure is raised again through the influence of the renin-angiotensin-aldosterone system.
In the kidney, the activation of the specific angiotensin 2 receptor results in the constriction of the smallest renal vessels. This process ensures that the kidney function remains constant even when blood pressure drops. In the adrenal gland, angiotensin 2 has no direct influence on vascular or muscle cells.
Instead, the tissue hormone unfolds its effect there by stimulating the release of two other messenger substances, aldosterone and adrenaline. In the pituitary gland (lat. pituitary gland), too, an increased release of another hormone is triggered after angiotensin 2 binds to its receptor.
It is also assumed that the sensation of thirst can be controlled by the release of angiotensin 2. In general, the described functions of the tissue hormone angiotensin 2 can be summarised as a blood pressure-increasing effect. Angiotensin 2 in its actual form cannot be excreted by the organism.
Rather, the tissue hormone must be cleaved by special enzymes (aminopeptidases) after it has exerted its effect and thus inactivated. In this context, it must be taken into account that the intermediate products produced during the degradation process can also have an influence on the tissue hormone. – Vascular system
- Kidneys
- Adrenal glands and
- CNS (Central Nervous System)
The renin-angiotensin-aldosterone system in general and the tissue hormone angiotensin 2 in particular offers drug manufacturers a suitable target for the treatment of many diseases. All common drugs are generally produced and used to lower blood pressure (antihypertensives) and to relieve the heart. A rough distinction is made between two types of medication: Among the most important side effects of ACE inhibitors and AT1 receptor antagonists are: occur
- ACE inhibitors (inhibit the formation of angiotensin 2)
- AT1- receptor antagonists (block specific receptor of the hormone and thus prevent angiotensin 2-receptor interaction)
- Chronic chesty cough
- Hypotension
- Headaches
- Tiredness and
- Circulatory problems
- Drugs High blood pressure
- Angiotensin-2 antagonists
- Angiotensin 2 Action
- ACE inhibitors
- ACE inhibitors Side effects