Changes

The RAAS is activated whenever blood flow through the kidneys is reduced and when there are sodium losses in conditions such as diarrhoes, 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.   

The RAAS is activated whenever blood flow through the kidneys is reduced and when there are sodium losses in conditions such as diarrhoes, 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.   

===The System===

==Physiology of the RAAS==

[[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 by inducing constriction of arterioles, which increases vascular resistance, and constricting veins which reduces vascular volume. In this section we cover its effects on and through the kidneys.

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 by inducing constriction of 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 2 on Blood Pressure====

==Effects of Angiotensin 2 on Blood Pressure==

'''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 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 | ADH]] to help increase blood volume. The RAAS allows pressure to return to 50% of baseline within 15 minutes of a significant haemorrhage occuring.

'''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 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 | ADH]] to help increase blood volume. The RAAS allows pressure to return to 50% of baseline within 15 minutes of a significant haemorrhage occuring.

====Effects of Angiotensin 2 on GFR====

==Effects of Angiotensin 2 on GFR==

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.   

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=====

===Advantages of Constriction of the Efferent Arteriole===

* 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.)

* 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 kidneys can tolerate the reduced perfusion allowing blood to be prioritised to organs which need it like the brain and heart.

* The amount of waste excreted is variable with GFR.  Thanks to the normalised GFR the excretion of waste products such as urea is maintained.

* 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====

==Effects of Angiotensin 2 On Sodium==

* Induces insertion of Na⁺ channels into renal tubules via stimulation of AT₁ receptors

* Induces insertion of Na⁺ channels into renal tubules via stimulation of AT₁ receptors

* Proximal tubule:

* Proximal tubule: