Difference between revisions of "Aldosterone"
Jump to navigation
Jump to search
(→Action) |
|||
Line 45: | Line 45: | ||
* In cases of increased K<sup>+</sup> | * In cases of increased K<sup>+</sup> | ||
− | * Increased | + | * Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity increases the amount of K<sup>+</sup> in cells to reduce plasa 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 pottassium secretion | * Causes pottassium secretion | ||
− | ** Pottassium via apical leak channels | + | ** Stimulates Na<sup>+</sup> / K<sup>+</sup> ATPases in the basolateral membrane of the principal cells |
+ | ** Increased pottasium in the cells | ||
+ | ** Pottassium leaves via apical leak channels | ||
+ | ** Thanks to electro-chemical gradient | ||
* Very tightly regulated system | * Very tightly regulated system | ||
** Allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup> | ** Allows large increase in K<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup> |
Revision as of 16:24, 5 July 2008
Overview
- Steroid hormone
- Secreted from the zona glomerulosa of the adrenal cortex of the adrenal gland
- Mineralocorticoid
- Most important regulator of plasma pottassium
- Stimulated directly by increased plasma pottassium
- Also stimulated as part of the Renin-Angiotensin-Aldosterone System (RAAS)
Release
- Release is stimulated by 3 things
- Corticotropin (ACTH)
- Angiotensin 2
- K+
- 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 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 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
- 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+
- Increased Na+ / K+ ATPase pump activity increases the amount of K+ in cells to reduce plasa K+
- Generally not excreted
- However if plasma K+ is still high aldosterone is stimulated
- Causes pottassium secretion
- Stimulates Na+ / K+ ATPases in the basolateral membrane of the principal cells
- Increased pottasium in the cells
- Pottassium 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
- Hydrogen by proton secretory proteins