Difference between revisions of "Renin Angiotensin Aldosterone System"

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Also known as: '''''RAAS'''''
 
Also known as: '''''RAAS'''''
  
 
[[Image:RAS.jpg|right|thumb|300px|<small><center> Schematic of the RAAS ©RVC 2008</center></small>]]
 
[[Image:RAS.jpg|right|thumb|300px|<small><center> Schematic of the RAAS ©RVC 2008</center></small>]]
 +
 
==Introduction==
 
==Introduction==
The RAAS allows an animal’s salt intake to vary without any great affect on ECF volume or arterial pressure. If an animal’s salt intake increased 50x its blood pressure would only increase 5-6mmHg
 
* Without the RAAS it would go up 10x that amount!
 
  
===The System===
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The RAAS is activated whenever blood flow through the kidneys is reduced, and when there are sodium losses in conditions such as diarrhoea, vomiting or excessive sweating. These losses reduce extracellular fluid volume, and this in turn reduces arterial blood pressure, which triggers the RAAS system through several different mechanisms. 
 +
 
 +
==RAAS Activation==
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[[Image:raasflowdefap.jpg|right|thumb|275px|<small><center>The Mechanism Behind the RAAS </center></small>]]
 
[[Image:raasflowdefap.jpg|right|thumb|275px|<small><center>The Mechanism Behind the RAAS </center></small>]]
 
[[Image:raasflowsumap.jpg|right|thumb|250px|<small><center>Summary of the purpose of the RAAS</center></small>]]
 
[[Image:raasflowsumap.jpg|right|thumb|250px|<small><center>Summary of the purpose of the RAAS</center></small>]]
In the event of blood pressure dropping [[Kidney Endocrine Function - Anatomy & Physiology#Renin|Renin]] is secreted due to the decreased stretch of the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Juxtaglomerular Cells|'''juxtaglomerular cells''']] and an increased sympathetic stimulation triggered by the decreased activation of arterial baroreceptors.  This enzyme cleaves the alpha glycoprotein '''Angiotensinogen''' which is released from the [[Liver - Anatomy & Physiology|liver]].  This produces '''Angiotensin 1''' which is further converted by [[Angiotensin Converting Enzyme(ACE) - Renal Anatomy & Physiology|'''Angiotensin Converting Enzyme''' (ACE)]] to '''Angiotensin 2''' mainly in the lungs but to a much lesser extent locally in the kidneys.  Angiotensin 2 then works to restore blood pressure.  In this section we cover its effects on and through the kidneys.
 
  
====Effects of Angiotensin 2 on Blood Pressure====
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In the event of blood pressure dropping, [[Kidney Endocrine Function - Anatomy & Physiology#Renin|renin]] is secreted due to the decreased stretch of the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Juxtaglomerular Cells|'''juxtaglomerular cells''']] and an increased sympathetic stimulation, triggered by the decreased activation of arterial baroreceptors. This enzyme cleaves the alpha glycoprotein, '''angiotensinogen''', which is released from the [[Liver - Anatomy & Physiology|liver]]. This produces '''angiotensin 1''', which is further converted by [[Angiotensin Converting Enzyme|'''Angiotensin Converting Enzyme''' (ACE)]] to '''angiotensin II''', mainly in the lungs but to a much lesser extent locally in the kidneys. Angiotensin II then works to restore blood pressure by inducing constriction of peripheral vessels (arterioles), which increases vascular resistance, and constricting veins which reduces vascular volume. In this section, we cover its effects on and through the kidneys.
'''Angiotensin 2''' acts on '''AT1 receptors''' to stimulate the release of '''[[Aldosterone]]''' from the [[Adrenal Glands - Anatomy & Physiology#Adrenal Glands|Zona Glomerulosa]] of the adrenal glands. This mineralocorticoid increases the reabsorption of sodium and therefore water and chloride from the distal tubule thus helping to increase blood volume and pressure. It also stimulates the thirst center and increases the secretion of [[Pituitary Gland - Anatomy & Physiology #Posterior Pituitary Gland | ADH]] to help increase blood volume. Thanks to the RAAS pressure can return to 50% baseline within 15 minutes of haemorrhage.
+
 
 +
==Effects of Angiotensin II on Blood Pressure==
 +
 
 +
'''Angiotensin II''' acts on '''AT1 receptors''' to stimulate the release of '''[[Aldosterone|aldosterone]]''' from the [[Adrenal Glands - Anatomy & Physiology#Adrenal Glands|zona glomerulosa]] of the adrenal glands. This mineralocorticoid increases the excretion of potassium and the reabsorption of sodium, and therefore water and chloride from the distal tubule of the kidney, thus helping to increase blood pressure and volume. It also stimulates the thirst center, and increases the secretion of [[Pituitary Gland - Anatomy & Physiology #Posterior Pituitary Gland |anti-diuretic hormone (ADH)]] to help increase blood volume by making the distal convoluted tubule and the collecting duct permeable to water. The RAAS allows pressure to return to 50% of baseline within 15 minutes of a significant haemorrhage occurring.
 +
 
 +
==Effects of Angiotensin II on GFR==
 +
 
 +
If blood pressure drops then [[Glomerular Apparatus and Filtration - Anatomy & Physiology#Glomerular Filtration Rate|glomerular filtration rate (GFR)]] also drops, due to reduced blood flow through the kidneys. To restore homeostasis, contraction of the efferent arteriole occurs in response to angiotensin II and the pressure difference between the afferent and efferent arterioles increases, creating greater filtration pressure. Therefore, when blood pressure falls, there is minimum alteration of GFR. The increased renal resistance to blood flow and the maintained GFR has many advantageous effects. 
 +
 
 +
===Advantages of Angiotensin II induced Vasoconstriction===
 +
 
 +
Increased total peripheral resistance helps to return blood pressure towards normal. (Angiotensin II also has vasoconstrictive effects in multiple organs.) The reduced perfusion of the kidneys allows blood to be diverted to the brain and heart. The constriction of the efferent arterioles also reduces hydrostatic pressure in the [[Glomerular Apparatus and Filtration - Anatomy & Physiology#Pressure in the Peritubular Capillaries|peritubular capillaries]], increasing reabsorption of water and salt and helping to restore the extracellular fluid (ECF) and normalising blood pressure. The amount of waste excreted is linked to the GFR. Maintaining GFR, permits the excretion of waste products such as urea to be maintained.
 +
 
 +
==Effects of Angiotensin II On Sodium==
 +
 
 +
Induces insertion of Na<sup>+</sup> channels into renal tubules via stimulation of AT<sub>1</sub> receptors. These occur in:
 +
 
 +
1. The proximal tubule, with the addition of:
 +
 
 +
Apical - Na<sup>+</sup>/H<sup>+</sup> exchangers and basolateral Na<sup>+</sup>(HCO<sub>3</sub><sup>-</sup>)<sub>3</sub> and Na<sup>+</sup>K<sup>+</sup>ATPase.
 +
 
 +
2. The thick ascending limb, with the addition of:
 +
 
 +
Apical Na<sup>+</sup>/H<sup>+</sup> exchangers and Na<sup>+</sup>K<sup>+</sup>2Cl<sup>-</sup> symporter.
 +
 
 +
3. The collecting ducts, with the addition of:
  
====Effects of Angiotensin 2 on GFR====
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Epithelial Na<sup>+</sup> channels.
If blood pressure drops then [[The Formation of the Filtrate by the Glomerular Apparatus- Anatomy & Physiology#Glomerular Filtration Rate|GFR]] also drops due to a reduced blood flow through the kidneys. Therefore it is important to prevent this.  If contraction of the efferent arteriole occurs then the pressure difference between the afferent and efferent arterioles increases creating a greater filtration pressure.  This effect is mediated by Angiotensin 2 and means that when blood pressure falls there is minimum alteration of GFR.  Blood flow which is already reduced due to the reduced pressure will then be further reduced by the increase in resistance.  This increased renal resistance to blood flow and the maintained GFR has many advantageous effects. 
 
  
=====Advantages of Constriction of the Efferent Arteriole=====
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Angiotensin II also stimulates the release of '''Aldosterone'''.
* If you increase the resistance in the kidneys you contribute to increasing total peripheral resistance.  This helps to return blood pressure towards normal.  (Angiotensin 2 also has vasoconstrictive effects in other organs.)
 
* The kidneys can tolerate the reduced perfusion allowing blood to be prioritised to organs which need it like the brain and heart.
 
* The constriction of the efferent arterioles also reduces hydrostatic pressure in the [[The Formation of the Filtrate by the Glomerular Apparatus- Anatomy & Physiology#Pressure in the Peritubular Capillaries| Peritubular Capillaries]] this increases reabsorption of water and salt thus helping to restore the ECF and thus helps to normalise blood pressure.
 
* The amount of waste excreted is variable with GFR.  Thanks to the normalised GFR the excretion of waste products such as urea is maintained.
 
  
====Effects of Angiotensin 2 On Sodium====
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{{Template:Learning
* Induces insertion of Na<sup>+</sup> channels into renal tubules via stimulation of AT<sub>1</sub> receptors
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|flashcards = [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|Hormonal Regulators of the Kidney]]
* Proximal tubule:
+
}}
** Apical - Na<sup>+</sup>/H<sup>+</sup> exchangers
 
** Basolateral Na<sup>+</sup>(HCO<sub>3</sub><sup>-</sup>)<sub>3</sub> and Na<sup>+</sup>K<sup>+</sup>ATPase
 
* Thick ascending limb
 
** Apical Na<sup>+</sup>/H<sup>+</sup> exchangers and Na<sup>+</sup>K<sup>+</sup>2Cl<sup>-</sup> symporter
 
* Collecting Duct
 
** Epithelial Na<sup>+</sup> channel
 
* Also stimulates '''Aldosterone'''
 
  
==Revision==
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==Webinars==
Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself.
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<rss max="10" highlight="none">https://www.thewebinarvet.com/urogenital-and-reproduction/webinars/feed</rss>
  
[[Category:Urinary System - Anatomy & Physiology]][[Category:Endocrine System - Anatomy & Physiology]]
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[[Category:Kidney Hormonal Regulators]][[Category:Endocrine System - Anatomy & Physiology]]
[[Category:Image Review]]
 
 
[[Category:Blood Pressure]]
 
[[Category:Blood Pressure]]
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[[Category:A&P Done]]
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[[Category:Cardiology Section]]

Latest revision as of 16:51, 3 January 2023


Also known as: RAAS

Schematic of the RAAS ©RVC 2008

Introduction

The RAAS is activated whenever blood flow through the kidneys is reduced, and when there are sodium losses in conditions such as diarrhoea, vomiting or excessive sweating. These losses reduce extracellular fluid volume, and this in turn reduces arterial blood pressure, which triggers the RAAS system through several different mechanisms.

RAAS Activation

The Mechanism Behind the RAAS
Summary of the purpose of the RAAS

In the event of blood pressure dropping, renin is secreted due to the decreased stretch of the juxtaglomerular cells and an increased sympathetic stimulation, triggered by the decreased activation of arterial baroreceptors. This enzyme cleaves the alpha glycoprotein, angiotensinogen, which is released from the liver. This produces angiotensin 1, which is further converted by Angiotensin Converting Enzyme (ACE) to angiotensin II, mainly in the lungs but to a much lesser extent locally in the kidneys. Angiotensin II then works to restore blood pressure by inducing constriction of peripheral vessels (arterioles), which increases vascular resistance, and constricting veins which reduces vascular volume. In this section, we cover its effects on and through the kidneys.

Effects of Angiotensin II on Blood Pressure

Angiotensin II acts on AT1 receptors to stimulate the release of aldosterone from the zona glomerulosa of the adrenal glands. This mineralocorticoid increases the excretion of potassium and the reabsorption of sodium, and therefore water and chloride from the distal tubule of the kidney, thus helping to increase blood pressure and volume. It also stimulates the thirst center, and increases the secretion of anti-diuretic hormone (ADH) to help increase blood volume by making the distal convoluted tubule and the collecting duct permeable to water. The RAAS allows pressure to return to 50% of baseline within 15 minutes of a significant haemorrhage occurring.

Effects of Angiotensin II on GFR

If blood pressure drops then glomerular filtration rate (GFR) also drops, due to reduced blood flow through the kidneys. To restore homeostasis, contraction of the efferent arteriole occurs in response to angiotensin II and the pressure difference between the afferent and efferent arterioles increases, creating greater filtration pressure. Therefore, when blood pressure falls, there is minimum alteration of GFR. The increased renal resistance to blood flow and the maintained GFR has many advantageous effects.

Advantages of Angiotensin II induced Vasoconstriction

Increased total peripheral resistance helps to return blood pressure towards normal. (Angiotensin II also has vasoconstrictive effects in multiple organs.) The reduced perfusion of the kidneys allows blood to be diverted to the brain and heart. The constriction of the efferent arterioles also reduces hydrostatic pressure in the peritubular capillaries, increasing reabsorption of water and salt and helping to restore the extracellular fluid (ECF) and normalising blood pressure. The amount of waste excreted is linked to the GFR. Maintaining GFR, permits the excretion of waste products such as urea to be maintained.

Effects of Angiotensin II On Sodium

Induces insertion of Na+ channels into renal tubules via stimulation of AT1 receptors. These occur in:

1. The proximal tubule, with the addition of:

Apical - Na+/H+ exchangers and basolateral Na+(HCO3-)3 and Na+K+ATPase.

2. The thick ascending limb, with the addition of:

Apical Na+/H+ exchangers and Na+K+2Cl- symporter.

3. The collecting ducts, with the addition of:

Epithelial Na+ channels.

Angiotensin II also stimulates the release of Aldosterone.


Renin Angiotensin Aldosterone System Learning Resources
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Flashcards
Test your knowledge using flashcard type questions
Hormonal Regulators of the Kidney


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