Difference between revisions of "Aldosterone"
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− | # | + | 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 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<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''' 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 | ||
+ | |||
+ | ===Action=== | ||
+ | |||
+ | * Diffuses across the cell membrane - lipophillic (essentially steroidal) | ||
+ | * Of the principal cells of [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Distal Tubule| distal tubule]] and [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Collecting Duct| 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<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 | ||
+ | ** '''Angiotensin 2''' and '''Aldosterone''' affect sodium but they also affect ECF volume so only quantity affected not concentration | ||
+ | ** [[Pituitary Gland - Anatomy & Physiology #Posterior Pituitary Gland | ADH]] and thirst response also work together to dilute the ECF if concentrations of sodium are 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<sup>+</sup> | ||
+ | * Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity increases the amount of K<sup>+</sup> in cells to reduce plasma K<sup>+</sup> | ||
+ | * Generally not excreted | ||
+ | * However if plasma K<sup>+</sup> is still high aldosterone is stimulated | ||
+ | * Causes potassium secretion | ||
+ | ** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells | ||
+ | ** Increased potassium in the cells | ||
+ | ** Potassium 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===== | ||
+ | |||
+ | * 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== | ||
+ | |||
+ | Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself. | ||
+ | |||
+ | [[Category:Urinary System - Anatomy & Physiology]][[Category:Endocrine System - Anatomy & Physiology]] |
Revision as of 14:02, 13 September 2010
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 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 sodium 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 are 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 plasma K+
- Generally not excreted
- However if plasma K+ is still high aldosterone is stimulated
- Causes potassium secretion
- Stimulates Na+ / K+ ATPases in the basolateral membrane of the principal cells
- Increased potassium in the cells
- Potassium 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
Revision
Use the flash card revision resource for this section to test yourself.