Difference between revisions of "Aldosterone"
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# [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]] | # [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| Angiotensin 2]] | ||
# K<sup>+</sup> | # K<sup>+</sup> | ||
− | * Its release is inhibited by [[Atrial | + | * Its release is inhibited by [[Atrial Natriuretic 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 | * 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 |
Revision as of 15:24, 11 August 2008
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Overview
Aldosterone is a steroid hormone which is secreted from the zona glomerulosa of the adrenal gland. It has a mineralocorticoid activitiy and is the most important regulator of plasma pottasium. When plasma pottasium increases increased stimulation of aldosterone occurs directly and as a result of Renin-Angiotensin-Aldosterone System (RAAS). It is also the most important regulator of sodium excretion.
Release
- Release is stimulated by 3 things
- Corticotropin (ACTH)
- Angiotensin 2
- K+
- Its release is inhibited by Atrial Natriuretic 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