Difference between revisions of "Aldosterone"
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==Overview== | ==Overview== | ||
− | Aldosterone is a steroid hormone which is secreted from the zona glomerulosa of the adrenal gland. It has a mineralocorticoid | + | 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) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]]. It is also the most important regulator of sodium excretion. |
==Release== | ==Release== | ||
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* Total quantity of sodium is conserved not the actual plasma concentration | * 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 | ** 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 | + | ** [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| 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 | + | ** 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 | * 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 | * At maximal secretion no significant amount of sodium would be excreted | ||
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* In cases of increased K<sup>+</sup> | * 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 | + | * 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 | * Generally not excreted | ||
* However if plasma K<sup>+</sup> is still high aldosterone is stimulated | * However if plasma K<sup>+</sup> is still high aldosterone is stimulated | ||
− | * Causes | + | * Causes potassium secretion |
** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells | ** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells | ||
− | ** Increased | + | ** Increased potassium in the cells |
− | ** | + | ** Potassium leaves via apical leak channels |
** Thanks to electro-chemical gradient | ** Thanks to electro-chemical gradient | ||
* Very tightly regulated system | * Very tightly regulated system |
Revision as of 09:27, 22 August 2008
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Overview
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