Difference between revisions of "Aldosterone"
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* Also stimulated as part of the [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]] | * Also stimulated as part of the [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]] | ||
| + | ==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 | ||
==Action== | ==Action== | ||
| − | * Works by altering gene transcription | + | * 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 | ** Affects ATP levels | ||
| Line 20: | Line 34: | ||
* Affects sodium entry and transport | * Affects sodium entry and transport | ||
| − | * Increases sodium | + | * 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 by proton secretory proteins | ** Hydrogen by proton secretory proteins | ||
Revision as of 19:47, 4 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