Difference between revisions of "Aldosterone"
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+ | <big><center>[[Kidney - Electrolyte Balance|'''BACK TO ELECTROLYTE BALANCE''']]</center></big> | ||
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− | + | ==Overview== | |
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+ | * Steroid hormone | ||
+ | * 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== | ==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 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 | |
− | + | * 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 | |
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− | 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]] | ||
+ | * 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 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=== | |
− | + | * In cases of increased K<sup>+</sup> | |
− | + | * Increased sodium 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 | ||
+ | ** 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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Revision as of 14:08, 5 July 2008
Overview
- Steroid hormone
- 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)
Release
- Release is stimulated by 3 things
- Corticotropin (ACTH)
- Angiotensin 2
- K+
- 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 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
- 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 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
- 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
- In cases of increased K+
- Increased sodium 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
- Pottassium via apical leak channels in the principal cells
- Very tightly regulated system
- Allows large increase in K+ to have a miniscule effect on plasma K+
Hydrogen
- Hydrogen by proton secretory proteins