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| ===Introduction=== | | ===Introduction=== |
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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|Renin-Angiotensin-Aldosterone System (RAAS)]]. It is also the most important regulator of sodium excretion. | + | 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 also as a result of the [[Renin Angiotensin Aldosterone System|Renin-Angiotensin-Aldosterone System (RAAS)]]. Aldosterone is also the most important regulator of sodium excretion. |
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| ===Release=== | | ===Release=== |
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− | * Release is stimulated by 3 things
| + | The release of aldosterone is stimulated by 3 things; |
− | # Corticotropin (ACTH)
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− | # Angiotensin 2
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− | # K<sup>+</sup>
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− | * Its release is inhibited by Atrial Natriuretic Peptide
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− | * Most increases in the concentration of aldosterone however can be explained by increases in the [[Renin Angiotensin Aldosterone System|'''Renin-Angiotensin-Aldosterone System''']] and therefore angiotensin 2 and/or by increases in K<sup>+</sup> concentration
| + | 1. '''Corticotropin (ACTH)''' |
− | * Only in severe fluid loss does ACTH significantly stimulate the release of aldosterone
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− | * ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion
| + | 2. '''Angiotensin 2''' |
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| + | 3. '''K<sup>+</sup>''' |
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| + | The release of aldosterone is inhibited by '''Atrial Natriuretic Peptide'''. |
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| + | Most increases in the concentration of aldosterone can be explained by increases in the [[Renin Angiotensin Aldosterone System|'''Renin-Angiotensin-Aldosterone System''']] and therefore, angiotensin 2 and/or by increases in K<sup>+</sup> concentration. ACTH only significantly stimulates the release of aldosterone during severe fluid loss. ANP is secreted in response to sodium/water loading and therefore inhibits aldosterone secretion. |
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| ===Action=== | | ===Action=== |
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− | * Diffuses across the cell membrane - lipophillic (essentially steroidal)
| + | Aldosterone diffuses across the cell membrane of the principal cells of the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Distal Tubule|distal tubule]] and the [[Reabsorption and Secretion Along the Distal Tubule and Collecting Duct - Anatomy & Physiology#Collecting Duct|collecting duct]]. It binds to cytoplasmic receptors and works by altering the gene transcription and increasing the synthesis of proteins. It also affects ATP levels. |
− | * 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]]
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− | * Binds to cytoplasmic receptors
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− | * Works by altering gene transcription and increases synthesis of proteins
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− | ** Affects ATP levels
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| =====Sodium===== | | =====Sodium===== |
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− | * Affects sodium entry and transport
| + | Aldosterone affects sodium entry and transport. It increases the number of apical sodium channels, NaCl co-transporters and Na<sup>+</sup>K<sup>+</sup>ATPase. It also increases the activity of the hydrogen sodium exchanger in the apical membrane and increases membrane permeability and the sodium pump activity. When sodium is reabsorbed, water follows it so the volume of the plasma is altered rather than the concentration of the sodium changing. I.e. '''angiotensin 2''' and '''aldosterone''' affect sodium, but they also affect the ECF volume, so only the quantity is affected, not the concentration. |
− | * Increases number of apical sodium channels, NaCl co-transporters and Na<sup>+</sup>K<sup>+</sup>ATPase
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− | * Increases activity of the hydrogen sodium exchanger in the apical membrane
| + | [[Pituitary Gland - Anatomy & Physiology #Posterior Pituitary Gland |ADH]] and the thirst response also work together to dilute the ECF if the 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. |
− | * Increases membrane permeability
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− | * Increases sodium pump activity
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− | * Total quantity of sodium is conserved not the actual plasma concentration
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− | ** When sodium is reabsorbed water follows it so the volume of the plasma is altered rather than the concentration of sodium changing
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− | ** '''Angiotensin 2''' and '''Aldosterone''' affect sodium but they also affect ECF volume so only quantity affected not concentration
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− | ** [[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.
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− | * If there was no secretion of aldosterone a 20kg dog would excrete 15g per 24 hours
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− | * At maximal secretion no significant amount of sodium would be excreted
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| =====Potassium===== | | =====Potassium===== |
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− | * 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>. It is generally not excreted. However, if plasma K<sup>+</sup> is still, high aldosterone is stimulated. This causes potassium secretion and stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells. This results in increased potassium in the cells. Potassium then leaves via the apical leak channels , thanks to the electro-chemical gradient. This is a very tightly regulated system and allows large increase in K<sup>+</sup> to have a miniscule effect on plasma 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>
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− | * Generally not excreted
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− | * However if plasma K<sup>+</sup> is still high aldosterone is stimulated
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− | * Causes potassium secretion
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− | ** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells
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− | ** Increased potassium in the cells
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− | ** Potassium leaves via apical leak channels
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− | ** Thanks to electro-chemical gradient
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− | * Very tightly regulated system
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− | ** Allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup>
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| =====Hydrogen===== | | =====Hydrogen===== |
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− | * Increases hydrogen secretion by increasing Hydrogen ATPases in the apical membrane of the intercalated cells
| + | Aldosterone increases hydrogen secretion, by increasing Hydrogen ATPases in the apical membrane of the intercalated cells and by increasing the sodium hydrogen exchanger in the apical membrane of the principal cells. |
− | * Increases hydrogen secretion by increasing sodium hydrogen exchanger in the apical membrane of the principal cells
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− | ==Revision== | + | ==Links== |
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| Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself. | | Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself. |
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| [[Category:Kidney Hormonal Regulators]][[Category:Endocrine System - Anatomy & Physiology]] | | [[Category:Kidney Hormonal Regulators]][[Category:Endocrine System - Anatomy & Physiology]] |
− | [[Category:To Do - A&P]] | + | [[Category:To Do - AimeeHicks]] |