The renin -angiotensin -aldosterone system ( RAAS abbr. ) is a closed-loop system of various hormones and enzymes that control is essentially the salt and water balance of the body. In addition, RAAS is one of the body's most important blood pressure-regulating systems.
At the beginning of the renin -angiotensin -aldosterone cascade is the release of the enzyme renin from specialized units of the kidney tissue, called the juxtaglomerular apparatus. This is
- Of specialized cells of the blood vessel that supplies blood to the renal corpuscle ( glomerulus ) ( afferent or afferent vessel)
- From the so-called macula densa: specialized cells of the Harnkanälchens, which runs near the afferent,
- And of specialized connective tissue cells ( mesangial cells ).
The juxtaglomerular apparatus measures the blood pressure in the afferent, the salt content of the urine in the tubules and also reacts to signals from the autonomic nervous system and various hormones. Form myoepithelial cells of the afferent and save the renin granules. The following factors lead to an increased release of renin:
- Decreased blood flow to the renal corpuscle,
- Decreased blood pressure, measured by the blood pressure sensors ( baroreceptors ) of the afferent,
- Decrease the amount of liquid that is filtered in the glomeruli ( decreased glomerular filtration rate, GFR ),
- Decreased concentration of salt ( more precisely of chloride ions) in the urine (as measured by the salt sensors of the macula densa ),
- Activation of the sympathetic nervous system.
Renin is therefore always released when the blood pressure drops and / or a loss of salt and water (and hence blood volume) occurs.
The released into the renal renin acts as a proteolytic enzyme ( protease) and splits from the formed in the liver protein angiotensinogen the decapeptide angiotensin I from. This in turn is controlled by a further enzyme angiotensin converting enzyme ( or ACE) to the octapeptide angiotensin II. This is the end product of the enzyme cascade, which exerts its effect in the body.
First of angiotensin II causes a severe narrowing of the small blood vessels ( vasoconstriction ), which leads directly to an increase in blood pressure.
In the kidneys, angiotensin II leads to a narrowing especially those vessels that carry blood from the renal corpuscles ( glomeruli ) lead away, called Vasa efferentia. Thus, the vascular resistance in the drainage area of the glomeruli and thus the blood pressure in the capillary loops of the glomeruli increases. Since the pressure in the capillary loops in turn is the primary driving force for filtration, thanks to this mechanism, the filtration can be maintained in the glomeruli despite reduced renal perfusion.
In the adrenal cortex, angiotensin II leads to a release of the hormone aldosterone. This promotes the renal tubules return transport of sodium and water from the urine into the blood, causing the salt content of the blood and blood volume increase.
In the pituitary gland (hypophysis ) angiotensin II leads to an increased release of antidiuretic hormone ( ADH or vasopressin also called ). This hormone results in a reduced water excretion by the kidneys and therefore also serves the preservation of water.
In the central nervous system (CNS ) the different hormones lead to increased salt hunger and thirst solve out.
All of these effects in their entirety to an increase in salt and water content of the body, so that a larger volume of blood and ultimately in higher blood pressure. The hormones of the RAAS thus helping to compensate for drops in blood pressure by salt and volume losses initially by increased preservation of the remaining salt and water reserves to then by increased supply to correct ( of thirst and salt appetite ).
An overactivation of the system is prevented by negative feedback. Thus, a higher blood pressure, angiotensin II and also inhibit the release of aldosterone renin.
The renin -angiotensin -aldosterone system is the target of several drugs that are used, inter alia, the treatment of high blood pressure:
- Angiotensin converting enzyme ( ACE) inhibitors prevent the formation of angiotensin II
- Alternatively, the effect of angiotensin II may be blocked at its site of action, namely at the angiotensin receptor ( angiotensin receptor blockers or AT1 antagonists).
- Direct inhibitors of the enzyme renin ( renin inhibitor ).
- The effect of the secondary- released hormones (ADH and aldosterone ) can be pharmacologically influenced ( aldosterone antagonist ).
- Biochemical reaction
- Adrenal gland