Difference between revisions of "Aldosterone"

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Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself.
 
Use the [[Important Hormonal Regulators of the Kidney - Renal Flash Cards - Anatomy & Physiology|flash card revision resource]] for this section to test yourself.
  
[[Category:Urinary System - Anatomy & Physiology]][[Category:Endocrine System - Anatomy & Physiology]]
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[[Category:Kidney Hormonal Regulators]][[Category:Endocrine System - Anatomy & Physiology]]

Revision as of 16:26, 10 December 2010

Introduction

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). 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+
  • 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 activity of the hydrogen sodium exchanger in the apical membrane
  • Increases membrane permeability
  • Increases sodium pump activity
  • Total quantity of sodium is conserved not the actual plasma concentration
    • When sodium is reabsorbed water follows it so the volume of the plasma is altered rather than the concentration of sodium changing
    • Angiotensin 2 and Aldosterone affect sodium but they also affect ECF volume so only quantity affected not concentration
    • 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.
  • If there was no secretion of aldosterone a 20kg dog would excrete 15g per 24 hours
  • At maximal secretion no significant amount of sodium would be excreted
Potassium
  • In cases of increased K+
  • Increased Na+ / K+ ATPase pump activity increases the amount of K+ in cells to reduce plasma K+
  • Generally not excreted
  • However if plasma K+ is still high aldosterone is stimulated
  • Causes potassium secretion
    • Stimulates Na+ / K+ ATPases in the basolateral membrane of the principal cells
    • Increased potassium in the cells
    • Potassium 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
  • Increases hydrogen secretion by increasing Hydrogen ATPases in the apical membrane of the intercalated cells
  • Increases hydrogen secretion by increasing sodium hydrogen exchanger in the apical membrane of the principal cells

Revision

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