The renin-angiotensin-aldosterone system ( RAAS ) is a control circuit with various hormones and enzymes that essentially control the body's volume balance . In addition, RAAS is one of the most important blood pressure regulating systems in the body.
- from specialized cells of the blood vessel that supplies the kidney corpuscle ( glomerulus ) with blood ( vas afferens or supply vessel),
- from the so-called macula densa : specialized cells of the urinary tubule, which runs near the vas afferens,
- and from specialized cells of the connective tissue ( mesangial cells ).
The juxtaglomerular apparatus measures the blood pressure in the vas afferens, the salt content of the urine in the urinary tubules and also reacts to signals from the autonomic nervous system and various hormones. Myoepithelial cells of the vasa afferentia form and store the renin granules. The following influences lead to an increased release of renin:
- Decreased blood flow to the kidney corpuscle,
- decreased blood pressure, measured by the blood pressure sensors ( baroreceptors ) of the vas afferens,
- Decrease in the amount of fluid that is filtered out in the kidney corpuscles (decreased glomerular filtration rate GFR ),
- Decreased concentration of common salt (more precisely of chloride ions) in the urine (measured by the salt sensors in the macula densa),
- Activation of the sympathetic nervous system .
Renin is therefore always released when blood pressure drops (e.g. in the case of a stenosis of the renal artery) and / or a loss of table salt and water (and thus blood volume) occurs.
The renin released in the kidneys acts as a protein-splitting enzyme ( protease ) and splits the decapeptide angiotensin I from the protein angiotensinogen formed in the liver . This in turn is converted into the octapeptide angiotensin II by another enzyme ( angiotensin converting enzyme or ACE) . This is the end product of the enzyme cascade, which unfolds its effect in the body.
Primarily, angiotensin II causes severe constriction of the fine blood vessels ( vasoconstriction ), which leads directly to an increase in blood pressure.
In the kidneys, angiotensin II leads to a narrowing of the vessels that carry blood away from the kidney corpuscles (glomeruli), the so-called vasa efferentia . This increases the vascular resistance in the outflow area of the glomeruli and thus also the blood pressure in the capillary loops of the kidney corpuscles. Since the pressure in the capillary loops is the primary driving force for the filtration, thanks to this mechanism, the filtration in the kidney corpuscles can be maintained despite reduced kidney blood flow.
In the adrenal cortex , angiotensin II releases the hormone aldosterone . This promotes the return of sodium and water from the urine to the blood in the kidney tubules, which increases the salt content of the blood and the blood volume.
In the pituitary gland ( pituitary gland ), angiotensin II leads to an increased release of the antidiuretic hormone (also called ADH or vasopressin ). This hormone leads to a reduced excretion of water by the kidneys and thus also serves to preserve water.
In the central nervous system (CNS), the various hormones lead to an increased hunger for salt and a feeling of thirst .
All of these effects in their totality lead to an increase in the salt and water content of the body, thus to a larger blood volume and thus ultimately to a higher blood pressure. The RAAS hormones thus help to compensate for drops in blood pressure due to salt and volume losses, initially by increasing the conservation of the remaining salt and water reserves, and then to correct them through increased intake (through thirst and salt hunger).
An excessive activation of the system is avoided by negative feedback . A higher blood pressure, angiotensin II and also aldosterone inhibit the release of renin.
The renin-angiotensin-aldosterone system is the target of various drugs that are used, among other things, to treat high blood pressure:
- Angiotensin converting enzyme inhibitors ( ACE inhibitors ) prevent the formation of angiotensin II.
- Alternatively, the action of angiotensin II can be blocked at its site of action, namely at the receptor ( angiotensin receptor blockers or AT1 antagonists ).
- Direct inhibitors of the enzyme renin ( renin inhibitors ).
- The effect of the secondarily released hormones (ADH and aldosterone) can also be influenced pharmacologically ( aldosterone antagonists ).
Overactivation can lead to secondary aldosteronism .
If too much renin is produced, hyperreninism can occur.
- M. Pacurari, R. Kafoury, PB Tchounwou, K. Ndebele: The Renin-Angiotensin-aldosterone system in vascular inflammation and remodeling. In: International journal of inflammation. Volume 2014, 2014, pp. 689360, doi : 10.1155 / 2014/689360 . PMID 24804145 . PMC 3997861 (free full text). .
- F. Viazzi, G. Leoncini, R. Pontremoli: Antihypertensive treatment and renal protection: the role of drugs-inhibiting the renin-angiotensin-aldosterone system. In: High blood pressure and cardiovascular prevention: the official journal of the Italian Society of Hypertension . Volume 20, Number 4, December 2013, pp. 273-282, doi : 10.1007 / s40292-013-0027-y . PMID 24092648 . PMC 3828492 (free full text). .