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==Overview==
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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) - Anatomy & Physiology | Renin-Angiotensin-Aldosterone System (RAAS)]].  It is also the most important regulator of sodium excretion.
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==Release==
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* Release is stimulated by 3 things
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# Corticotropin (ACTH)
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# [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| 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 (RAAS) - Anatomy & Physiology| Renin-Angiotensin-Aldosterone System]] and therefore angiotensin 2 and/or by increases in K<sup>+</sup> concentration
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* 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
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==Action==
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* Diffuses across the cell membrane - lipophillic (essentially steroidal)
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* Of the principal cells of [[Distal Tubule - Anatomy & Physiology| distal tubule]] and [[Collecting Duct - Anatomy & Physiology| 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===
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* Affects sodium entry and transport
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* 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
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* 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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** [[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
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** 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===
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* In cases of increased K<sup>+</sup>
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* 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===
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* Increases hydrogen secretion by increasing Hydrogen ATPases in the apical membrane of the intercalated cells
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* Increases hydrogen secretion by increasing sodium hydrogen exchanger in the apical membrane of the principal cells
 
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