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 Natiuretic Peptide]]
+
* 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
  1. Corticotropin (ACTH)
  2. Angiotensin 2
  3. K+
  • 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