View source for Renin-angiotensin system

__NOTOC__
{{SI}}
{{CMG}}

{{SK}} RAS, RAAS

==Overview==
The '''renin-angiotensin system''' (RAS) or the '''renin-angiotensin-aldosterone system''' (RAAS) is a hormone system that helps regulate long-term [[blood pressure]] and [[extracellular fluid|extracellular volume]] in the body.

==Activation==
The system can be activated when there is a loss of [[blood]] volume or a drop in [[blood pressure]] (such as in a [[hemorrhage]]).  

# If the perfusion of the [[juxtaglomerular apparatus]] in the [[kidney]]s decreases, then the juxtaglomerular cells release the [[enzyme|enzyme]] [[renin]]. 
# Renin cleaves an inactive [[peptide]] called ''[[angiotensinogen]]'', converting it into ''[[angiotensin|angiotensin I]]''.  
# Angiotensin I is then converted to ''[[angiotensin|angiotensin II]]'' by [[angiotensin-converting enzyme]] (ACE),<ref>{{GeorgiaPhysiology|7/7ch09/7ch09p16}}</ref> which is found mainly in [[lung]] [[capillaries]].
# Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as an [[endocrine system | endocrine]], [[autocrine signalling | autocrine]]/[[paracrine signalling | paracrine]], and [[intracrine]] hormone.


[[Image:Renin-angiotensin-aldosterone system.png|thumb|center|500px|Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus]]

==Effects==
[[Angiotensin I]] may have some minor activity, but angiotensin II is more potent. Angiotensin II has a variety of effects on the body:
*''Throughout the body'', it is a potent [[vasoconstrictor]].
*''In the [[kidney]]s'', it constricts [[Glomerulus (kidney)|glomerular]] [[arteriole]]s, having a greater effect on [[efferent arterioles]] than afferent. As with most other capillary beds in the body, the constriction of [[afferent arterioles]] increases the arterioler resistance, raising [[systemic circulation|systemic]] [[arterial blood pressure]] and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, Angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The [[glomerular filtration rate]] (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow.
*''In the [[adrenal cortex]]'', it acts to cause the release of ''[[aldosterone]]''. Aldosterone acts on the tubules (i.e. the [[distal convoluted tubule]]s and the [[renal cortex|cortical]] [[collecting duct]]s) in the kidneys, causing them to reabsorb more [[sodium]] and water from the [[urine]]. Potassium is secreted into the tubule in exchange for the sodium, which is reabsorbed. Aldosterone also acts on the [[central nervous system]] to increase a person's appetite for salt, and to make them feel thirsty.
*''Release of Anti Diuretic Hormone (ADH) -- also called [[vasopressin]] -- ADH is made in the hypothalamus. ADH is stored and released from the pituitary gland.

These effects directly act to increase the amount of fluid in the blood, making up for a loss in volume, and to increase blood pressure.

==Clinical significance==
The renin-angiotensin system is often manipulated clinically to treat [[high blood pressure]].  
* [[ACE inhibitor|Inhibitors of angiotensin-converting enzyme]] (ACE inhibitors) are often used to reduce the formation of the more potent angiotensin II. Captopril is an example of an ACE inhibitor.
* Alternatively, [[angiotensin II receptor antagonist|angiotensin receptor blockers]] (ARBs) can be used to prevent angiotensin II from acting on [[angiotensin receptor]]s.
* A new drug called [[Aliskiren]] is being released in 2007 which directly inhibits renin.

==Other uses of ACE==
Interestingly, [[ACE]] cleaves a number of other peptides, and in this capacity is an important regulator of the [[kinin-kallikrein system]].

== Fetal renin-angiotensin system ==
In the [[fetus]], the renin-angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower &mdash; this is due to the limited pulmonary blood flow, preventing ACE (found predominantly in the pulmonary circulation) from having its maximum effect.

==References==
<references/>

==External links==
* {{MeshName|Renin-Angiotensin+System}}

{{Cardiovascular physiology}}

[[da:Renin-angiotensin-aldosteron-systemet]]
[[de:Renin-Angiotensin-Aldosteron-System]]
[[fr:Système rénine-angiotensine-aldostérone]]
[[he:מערכת הרנין-אנגיוטנסין-אלדוסטרון]]
[[it:Sistema renina-angiotensina]]
[[nl:Bloeddrukregulatie]]
[[pl:RAA]]
[[pt:Sistema renina-angiotensina]]
[[ru:Ренин-ангиотензиновая система]]
[[sk:Systém renín-angiotenzín-aldosterón]]
[[sv:Renin-angiotensinsystemet]]

[[Category:Cardiovascular system]]
[[Category:Cardiology]]
[[Category:Endocrinology]]
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}