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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 |
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| | * Affects sodium entry and transport | | * Affects sodium entry and transport |
| − | * Increases sodium re-uptake to a small degree in distal convoluted tubule | + | * 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> |
| | | | |
| − | ===Pottassium and Hydrogen=== | + | ===Hydrogen=== |
| | | | |
| − | * Causes pottassium and hydrogen secretion
| |
| − | ** Pottassium via apical leak channels
| |
| | ** Hydrogen by proton secretory proteins | | ** Hydrogen by proton secretory proteins |