View source for The renin-angiotensin-aldosterone system

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The '''Renin-angiotensin-aldosterone system''' (RAAS, renin-angiotensin-aldosterone axis) is one of the main '''neurohumoral''' regulators of '''physiological [[Homeostasis|homeostasis]]'''. The primary stimulus for its activation is the outflow of '''[[renin]]''' from juxtaglomerular cells, located in the media of afferent renal arterioles. This can happen based on:

*decreased '''blood flow''' through afferent arteriole (eg [[hypotension]] of various etiologies, renal artery stenosis);
*reduction of '''NaCl''' supply to the macula densa region of the distal tubule;
*activation of '''β<sub>1</sub>-adrenoreceptors''' in the region of juxtaglomerular cells.[[File:Renin-angiotensin-aldosterone system.svg|thumb|The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS)]]

Renin secretion is also '''stimulated'''' by [[prostaglandins]] (PGI2, PGE2). On the other hand, renin secretion is '''inhibited''' by [[Cardioinhibitors|β-blockers]]. 

==Mechanisms of transformations==
The main function of renin is the cleavage of the decapeptide '''angiotensin I''' (AGI) from '''angiotensinogen'''. Histidine and leucine in positions 9 and 10 are subsequently cleaved from angiotensin I by angiotensin-converting enzyme (ACE). This results in the octapeptide angiotensin II (AGII). ''Conversion diagram and function of AGII see picture''.

#AGII causes significant '''vasoconstriction''' predominantly in the arteriolar blood stream, with a lesser intensity it also affects the veins. Vasoconstriction is most evident in the [[skin|skin]] and [[kidneys|kidneys]]. At least, on the contrary, it affects the vessels of the [[brain|brain]] and muscles.
#In the kidneys, AGII leads to '''vas efferens constriction''' and by a not entirely clear mechanism, it ''increases sodium reabsorption in the proximal tubule''.
#In the adrenal cortex, it '''stimulates the release of [[aldosterone]]''', which subsequently potentiates the reabsorption of [[sodium]] and the excretion of [[potassium]] in the distal tubule and collecting duct.
#In the adrenal medulla, AGII '''facilitates the release of [[Catecholamine|catecholamines]]'''.
#Centrally '''increases sympathetic tone''' (stimulates the release of catecholamines from nerve endings).
#In the neurohypophysis, AGII '''stimulates the secretion of vasopressin'''' ([[ADH]]) with subsequent water retention. Most of these effects are mediated by the binding of AGII to the specific AT1-receptor.
#With a long-term increase in the concentration of AGII, its strong '''pro-oncogenic effect'''' is manifested - the growth of vascular smooth muscle cells and striated [[Myocardium|heart muscle]] is stimulated, the synthesis of [[collagen]] increases and the production increases [[Reactive forms of oxygen and nitrogen|superoxide radicals]].
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==Links==
===Related Articles===

*[[Kidneys]]
*[[Diuretics]]
*[[Kidney blood flow and its autoregulation]]
*[[Angiotensin converting enzyme inhibitors]]
*[[Angiotensin II receptor blockers]]

===Used literatury===
* {{Cite
| type = web
| surname1 = Martínková
| name1 = Dahlia
| surname2 = Michuda
| name2 = Stanislav
| surname3 = Cermanová
| name3 = Jolana
| url = https://www.lfhk.cuni.cz/farmakol/predn/bak/kapitoly/prednasky/kardio-bak.ppt/
| source_name = Selected chapters in clinical pharmacology for undergraduate studies
| subtitle = Cardiovascular system
| year = 2000
| cited = 2010-06-28
}}
</noinclude>

[[Category:Pathophysiology]]
[[Category:Biochemistry]]
[[Category:Physiology]]
[[Category:Physiology Practice]]
[[Category:Cardiology]]
[[Category:Pharmacology]]
[[Category:Nephrology]]