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Kidney Hormonal Regulators - Anatomy & Physiology (view source)
Revision as of 13:44, 3 September 2008
, 13:44, 3 September 2008no edit summary
** Epithelial Na<sup>+</sup> channel
** Epithelial Na<sup>+</sup> channel
* Also stimulates [[Aldosterone| Aldosterone]]
* Also stimulates [[Aldosterone| Aldosterone]]
==Aldosterone==
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
# Corticotropin (ACTH)
# Angiotensin 2
# K<sup>+</sup>
* 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
* 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 - Anatomy & Physiology| distal tubule]] and [[Collecting Duct - Anatomy & Physiology| 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<sup>+</sup>K<sup>+</sup>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
** [[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| 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<sup>+</sup>
* Increased Na<sup>+</sup> / K<sup>+</sup> ATPase pump activity increases the amount of K<sup>+</sup> in cells to reduce plasma K<sup>+</sup>
* Generally not excreted
* However if plasma K<sup>+</sup> is still high aldosterone is stimulated
* Causes potassium secretion
** Stimulates Na<sup>+</sup> / K<sup>+</sup> 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<sup>+</sup> to have a miniscule effect on plasma K<sup>+</sup>
=====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
<big>'''[[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| RAAS]]'''
<big>'''[[Renin-Angiotensin-Aldosterone System (RAAS) - Anatomy & Physiology| RAAS]]'''