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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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