Difference between revisions of "Aldosterone"
Jump to navigation
Jump to search
Fiorecastro (talk | contribs) |
(→Sodium) |
||
| (17 intermediate revisions by 4 users not shown) | |||
| Line 1: | Line 1: | ||
| + | {{toplink | ||
| + | |backcolour = C1F0F6 | ||
| + | |linkpage =Important Hormonal Regulators of the Kidney - Anatomy & Physiology | ||
| + | |linktext =IMPORTANT HORMONAL REGULATORS OF THE KIDNEY | ||
| + | |maplink = Urinary System (Content Map) - Anatomy & Physiology | ||
| + | |pagetype =Anatomy | ||
| + | }} | ||
| + | <br> | ||
| + | ==Overview== | ||
| − | + | Aldosterone is a steroid hormone which is secreted from the zona glomerulosa of the adrenal gland. It has a mineralocorticoid activitiy and is the most important regulator of plasma potasium. When plasma potasium increases increased stimulation of aldosterone occurs directly and as a result of [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]]. It is also the most important regulator of sodium excretion. | |
| − | |||
| − | |||
| − | Aldosterone is a | ||
==Release== | ==Release== | ||
| − | + | * Release is stimulated by 3 things | |
| − | + | # Corticotropin (ACTH) | |
| − | + | # [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]] | |
| − | + | # K<sup>+</sup> | |
| − | + | * Its release is inhibited by [[Atrial Natriuretic 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 | |
| − | + | * 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 | |
| − | |||
| − | Most increases in the concentration of aldosterone can be explained by increases in the [[Renin Angiotensin Aldosterone System| | ||
==Action== | ==Action== | ||
| − | + | * Diffuses across the cell membrane - lipophillic (essentially steroidal) | |
| + | * Of the principal cells of [[Distal Tubule - Anatomy & Physiology| distal tubule]] and [[Collecting Duct - Anatomy & Physiology| Collecting Duct]] | ||
| + | * Binds to cytoplasmic receptors | ||
| + | * Works by altering gene transcription and increases synthesis of proteins | ||
| + | ** Affects ATP levels | ||
===Sodium=== | ===Sodium=== | ||
| − | + | * Affects sodium entry and transport | |
| − | + | * Increases number of apical sodium channels, NaCl co-transporters and Na<sup>+</sup>K<sup>+</sup>ATPase | |
| − | + | * Increases activity of the hydrogen sodium exchanger in the apical membrane | |
| + | * Increases membrane permeability | ||
| + | * Increases sodium pump activity | ||
| + | * Total quantity of sodium is conserved not the actual plasma concentration | ||
| + | ** When sodium is reabsorbed water follows it so the volume of the plasma is altered rather than the concentration of sodium changing | ||
| + | ** [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]] and [[Aldosterone]] affect scodium but they also affect ECF volume so only quantity affected not concentration | ||
| + | ** ADH and thirst response also work together to dilute the ECF if 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=== | ===Potassium=== | ||
| − | Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity | + | * In cases of increased K<sup>+</sup> |
| + | * Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity increases the amount of K<sup>+</sup> in cells to reduce plasa K<sup>+</sup> | ||
| + | * Generally not excreted | ||
| + | * However if plasma K<sup>+</sup> is still high aldosterone is stimulated | ||
| + | * Causes pottassium secretion | ||
| + | ** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells | ||
| + | ** Increased pottasium in the cells | ||
| + | ** Pottassium leaves via apical leak channels | ||
| + | ** Thanks to electro-chemical gradient | ||
| + | * Very tightly regulated system | ||
| + | ** Allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup> | ||
===Hydrogen=== | ===Hydrogen=== | ||
| − | + | * Increases hydrogen secretion by increasing Hydrogen ATPases in the apical membrane of the intercalated cells | |
| − | + | * Increases hydrogen secretion by increasing sodium hydrogen exchanger in the apical membrane of the principal cells | |
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
| − | |||
Revision as of 18:51, 19 August 2008
|
Overview
Aldosterone is a steroid hormone which is secreted from the zona glomerulosa of the adrenal gland. It has a mineralocorticoid activitiy and is the most important regulator of plasma potasium. When plasma potasium increases increased stimulation of aldosterone occurs directly and as a result of Renin-Angiotensin-Aldosterone System (RAAS). It is also the most important regulator of sodium excretion.
Release
- Release is stimulated by 3 things
- Corticotropin (ACTH)
- Angiotensin 2
- K+
- Its release is inhibited by Atrial Natriuretic Peptide
- Most increases in the concentration of aldosterone however can be explained by increases in the Renin-Angiotensin-Aldosterone System and therefore angiotensin 2 and/or by increases in K+ concentration
- 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
- Diffuses across the cell membrane - lipophillic (essentially steroidal)
- Of the principal cells of distal tubule and Collecting Duct
- Binds to cytoplasmic receptors
- Works by altering gene transcription and increases synthesis of proteins
- Affects ATP levels
Sodium
- Affects sodium entry and transport
- Increases number of apical sodium channels, NaCl co-transporters and Na+K+ATPase
- Increases activity of the hydrogen sodium exchanger in the apical membrane
- Increases membrane permeability
- Increases sodium pump activity
- Total quantity of sodium is conserved not the actual plasma concentration
- When sodium is reabsorbed water follows it so the volume of the plasma is altered rather than the concentration of sodium changing
- Angiotensin 2 and Aldosterone affect scodium but they also affect ECF volume so only quantity affected not concentration
- ADH and thirst response also work together to dilute the ECF if 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
- In cases of increased K+
- Increased Na+ / K+ ATPase pump activity increases the amount of K+ in cells to reduce plasa K+
- Generally not excreted
- However if plasma K+ is still high aldosterone is stimulated
- Causes pottassium secretion
- Stimulates Na+ / K+ ATPases in the basolateral membrane of the principal cells
- Increased pottasium in the cells
- Pottassium leaves via apical leak channels
- Thanks to electro-chemical gradient
- Very tightly regulated system
- Allows large increase in K+ to have a miniscule effect on plasma K+
Hydrogen
- Increases hydrogen secretion by increasing Hydrogen ATPases in the apical membrane of the intercalated cells
- Increases hydrogen secretion by increasing sodium hydrogen exchanger in the apical membrane of the principal cells