Difference between revisions of "Aldosterone"

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<big><center>[[Kidney - Electrolyte Balance|'''BACK TO ELECTROLYTE BALANCE''']]</center></big>
 
  
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==Introduction==
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[[Image:aldosterone.png|right|thumb|250px Benjah 2006 Aldosterone 2D structure.]]
  
==Overview==
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Aldosterone is a '''steroid hormone''' which is secreted from the [[Adrenal Glands - Anatomy & Physiology#Function|'''zona glomerulosa''' of the adrenal gland]]. It has a mineralocorticoid activity and is the most important regulator of plasma potassium. When plasma potassium increases, increased stimulation of aldosterone occurs directly and also as a result of the [[Renin Angiotensin Aldosterone System|Renin-Angiotensin-Aldosterone System (RAAS)]]. Aldosterone is also the most important regulator of sodium excretion.
  
* Steroid hormone
+
==Release==
* Secreted from the zona glomerulosa of the adrenal cortex of the adrenal gland
 
* Mineralocorticoid
 
* Most important regulator of plasma pottassium
 
* Stimulated directly by increased plasma pottassium
 
* Also stimulated as part of the [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]]
 
  
==Release==
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The release of aldosterone is stimulated by 3 things;
 +
 
 +
1. '''Corticotropin (ACTH)'''
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 +
2. '''Angiotensin 2'''
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 +
3. '''K<sup>+</sup>'''
  
* Release is stimulated by 3 things
+
The release of aldosterone is inhibited by '''[[Atrial Natriuretic Peptide]] (ANP)'''.
# Corticotropin (ACTH)
 
# [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]]
 
# K<sup>+</sup>
 
* Its release is inhibited by Atrial Natiuretic Peptide
 
  
* Most increases in the concentration of aldosterone however can be explained by increases in the [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Renin-Angiotensin-Aldosterone System]] and therefore angiotensin 2 and/or by increases in K<sup>+</sup> concentration
+
Most increases in the concentration of aldosterone can be explained by increases in the [[Renin Angiotensin Aldosterone System|'''Renin-Angiotensin-Aldosterone System''']] and therefore, angiotensin 2 and/or by increases in K<sup>+</sup> concentration. ACTH only significantly stimulates the release of aldosterone during severe fluid loss. ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion.
* Only in severe fluid loss does ACTH significantly stimulate the release of aldosterone
 
* ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion
 
  
 
==Action==
 
==Action==
  
* Diffuses across the cell membrane - lipophillic (essentially steroidal)
+
Aldosterone diffuses across the cell membrane of the principal cells of the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Distal Tubule|distal tubule]] and the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Collecting Duct|collecting duct]]. It binds to cytoplasmic receptors and works by altering the gene transcription and increasing the synthesis of proteins. It also affects ATP levels.
* Of the principal cells of [[Distal Tubule - Anatomy & Physiology| distal tubule]]
 
* Binds to cytoplasmic receptors
 
* Works by altering gene transcription and increases synthesis of proteins
 
** Affects ATP levels
 
  
 
===Sodium===
 
===Sodium===
  
* Affects sodium entry and transport
+
Aldosterone affects sodium entry and transport. It increases the number of apical sodium channels, NaCl co-transporters and Na<sup>+</sup>K<sup>+</sup>ATPase. It also increases the activity of the hydrogen sodium exchanger in the apical membrane and increases membrane permeability and the sodium pump activity. When sodium is reabsorbed, water follows it so the volume of the plasma is altered rather than the concentration of the sodium changing. I.e. '''angiotensin 2''' and '''aldosterone''' affect sodium, but they also affect the extra cellular fluid (ECF) volume, so only the quantity is affected, not the concentration.
* Increases number of apical sodium channels, NaCl co-transporters and Na<sup>+</sup>K<sup>+</sup>ATPase
 
* Increases membrane permeability
 
* Increases sodium pump activity
 
* Total quantity of sodium is conserved not the actual plasma concentration
 
** This is because water follows sodium so the volume is altered according to the amount of sodium
 
** [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]] and aldosterone also affect ECF so only quantity affected not concentration
 
** ADH and thirst response also work together to dilute the ECF so although there is more NaCl the actual concentration is constant.
 
  
===Pottassium===
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[[Pituitary Gland - Anatomy & Physiology #Posterior Pituitary Gland |Antidiuretic hormone (ADH)]] and the thirst response also work together to dilute the ECF if the concentrations of sodium is high. So although there is more NaCl, the actual concentration is not really changed. If there was no secretion of aldosterone, a 20kg dog would excrete 15g per 24 hours. At maximal secretion, no significant amount of sodium would be excreted.
  
* In cases of increased K<sup>+</sup>
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===Potassium===
* Increased sodium pump activity increases the amount of K<sup>+</sup> in cells to reduce plasa K<sup>+</sup>
+
 
* Generally not excreted
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Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity, increases the amount of K<sup>+</sup> influx into cells to reduce plasma K<sup>+</sup>. Potassium is generally not excreted. However, if plasma K<sup>+</sup> is still, high aldosterone is stimulated. This causes potassium secretion and stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells. This results in increased potassium in the cells. Potassium then leaves via the apical leak channels , thanks to the electro-chemical gradient. This is a very tightly regulated system and allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup>.
* However if plasma K<sup>+</sup> is still high aldosterone is stimulated
 
* Causes pottassium secretion
 
** Pottassium via apical leak channels in the principal cells
 
* Very tightly regulated system
 
** Allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup>
 
  
 
===Hydrogen===
 
===Hydrogen===
  
** Hydrogen by proton secretory proteins
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Aldosterone increases hydrogen secretion, by increasing Hydrogen ATPases in the apical membrane of the intercalated cells and by increasing the sodium hydrogen exchanger in the apical membrane of the principal cells.
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{{Template:Learning
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|flashcards = [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|Important Hormonal Regulators of the Kidney]]
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}}
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==Webinars==
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<rss max="10" highlight="none">https://www.thewebinarvet.com/endocrinology/webinars/feed</rss>
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[[Category:Kidney Hormonal Regulators]][[Category:Endocrine System - Anatomy & Physiology]]
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[[Category:A&P Done]]

Latest revision as of 14:10, 9 January 2023

Introduction

250px Benjah 2006 Aldosterone 2D structure.

Aldosterone is a steroid hormone which is secreted from the zona glomerulosa of the adrenal gland. It has a mineralocorticoid activity and is the most important regulator of plasma potassium. When plasma potassium increases, increased stimulation of aldosterone occurs directly and also as a result of the Renin-Angiotensin-Aldosterone System (RAAS). Aldosterone is also the most important regulator of sodium excretion.

Release

The release of aldosterone is stimulated by 3 things;

1. Corticotropin (ACTH)

2. Angiotensin 2

3. K+

The release of aldosterone is inhibited by Atrial Natriuretic Peptide (ANP).

Most increases in the concentration of aldosterone can be explained by increases in the Renin-Angiotensin-Aldosterone System and therefore, angiotensin 2 and/or by increases in K+ concentration. ACTH only significantly stimulates the release of aldosterone during severe fluid loss. ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion.

Action

Aldosterone diffuses across the cell membrane of the principal cells of the distal tubule and the collecting duct. It binds to cytoplasmic receptors and works by altering the gene transcription and increasing the synthesis of proteins. It also affects ATP levels.

Sodium

Aldosterone affects sodium entry and transport. It increases the number of apical sodium channels, NaCl co-transporters and Na+K+ATPase. It also increases the activity of the hydrogen sodium exchanger in the apical membrane and increases membrane permeability and the sodium pump activity. When sodium is reabsorbed, water follows it so the volume of the plasma is altered rather than the concentration of the sodium changing. I.e. angiotensin 2 and aldosterone affect sodium, but they also affect the extra cellular fluid (ECF) volume, so only the quantity is affected, not the concentration.

Antidiuretic hormone (ADH) and the thirst response also work together to dilute the ECF if the concentrations of sodium is high. So although there is more NaCl, the actual concentration is not really changed. If there was no secretion of aldosterone, a 20kg dog would excrete 15g per 24 hours. At maximal secretion, no significant amount of sodium would be excreted.

Potassium

Increased Na+ / K+ ATPase pump activity, increases the amount of K+ influx into cells to reduce plasma K+. Potassium is generally not excreted. However, if plasma K+ is still, high aldosterone is stimulated. This causes potassium secretion and stimulates Na+ / K+ ATPases in the basolateral membrane of the principal cells. This results in increased potassium in the cells. Potassium then leaves via the apical leak channels , thanks to the electro-chemical gradient. This is a very tightly regulated system and allows large increase in K+ to have a miniscule effect on plasma K+.

Hydrogen

Aldosterone increases hydrogen secretion, by increasing Hydrogen ATPases in the apical membrane of the intercalated cells and by increasing the sodium hydrogen exchanger in the apical membrane of the principal cells.


Aldosterone Learning Resources
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Important Hormonal Regulators of the Kidney


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