Difference between revisions of "Potassium"
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*reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities. | *reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities. | ||
*increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities. | *increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities. | ||
− | |||
==Sources of Potassium== | ==Sources of Potassium== | ||
Potassium is absorbed via passive diffusion from the [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and via active transport from the [[Colon - Anatomy & Physiology|colon]]. It is regulated efficiently by [[Aldosterone|aldosterone]] levels and recovery from cellular breakdown during haemolysis or tissue damage. | Potassium is absorbed via passive diffusion from the [[Small Intestine Overview - Anatomy & Physiology|small intestine]] and via active transport from the [[Colon - Anatomy & Physiology|colon]]. It is regulated efficiently by [[Aldosterone|aldosterone]] levels and recovery from cellular breakdown during haemolysis or tissue damage. | ||
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The K<sup>+</sup> in the ECF only represents a very small amount of the total K<sup>+</sup> in the body; however its concentration is maintained within very strict parameters. The homeostasis of K<sup>+</sup> is managed by three routes: | The K<sup>+</sup> in the ECF only represents a very small amount of the total K<sup>+</sup> in the body; however its concentration is maintained within very strict parameters. The homeostasis of K<sup>+</sup> is managed by three routes: | ||
#Cellular translocation - this is the main method of control; it is an acute response that triggers Potassium movement either into or out of the cells. | #Cellular translocation - this is the main method of control; it is an acute response that triggers Potassium movement either into or out of the cells. | ||
− | #Renal excretion - this method makes up 90% of the chronic response (takes 4-6 hours to respond). It allows fine control and is regulated by [[Aldosterone| | + | #Renal excretion - this method makes up 90% of the chronic response (takes 4-6 hours to respond). It allows fine control and is regulated by [[Aldosterone|aldosterone]] |
− | #GI excretion - this route makes up the other 10% of the chronic response and becomes significant in cases of renal failure. This response is also influenced by [[Aldosterone]] | + | #GI excretion - this route makes up the other 10% of the chronic response and becomes significant in cases of renal failure. This response is also influenced by [[Aldosterone|aldosterone]] |
==Cellular Translocation== | ==Cellular Translocation== | ||
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* However net reabsorption / secretion of potassium occurs in the distal tubule and first part of collecting duct | * However net reabsorption / secretion of potassium occurs in the distal tubule and first part of collecting duct | ||
** Depends on bodies need | ** Depends on bodies need | ||
− | * Under the influence of [[Aldosterone]] | + | * Under the influence of [[Aldosterone|aldosterone]] |
* This is where the amount of potassium excreted is determined | * This is where the amount of potassium excreted is determined | ||
* Reabsorption occurs in the final part of the collecting duct | * Reabsorption occurs in the final part of the collecting duct | ||
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==Factors Influencing Potassium Excretion== | ==Factors Influencing Potassium Excretion== | ||
− | + | 1.Sodium: High sodium = increased potassium excretion and: | |
* More sodium into cells | * More sodium into cells | ||
* Increased Na<sup>+</sup> / K<sup>+</sup> ATPase | * Increased Na<sup>+</sup> / K<sup>+</sup> ATPase | ||
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* The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron | * The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron | ||
2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone. | 2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone. | ||
− | |||
[[Category:Electrolytes]] | [[Category:Electrolytes]] | ||
+ | [[Category:Minerals]] |
Latest revision as of 16:31, 12 April 2022
Introduction
Potassium is carefully regulated in the body - the consequences of altered Potassium levels are significant, including:
- reduced concentration of potassium in the ECF leads to plasma membranes hyperpolarization resulting in decreased firing of action potentials. This causes skeletal muscle weakness and cardiac abnormalities.
- increased concentration of potassium in the ECF leads to membrane depolarisation which is inappropriately triggered by action potentials. This can make the membrane insensitive to further stimulation causing cardiac abnormalities.
Sources of Potassium
Potassium is absorbed via passive diffusion from the small intestine and via active transport from the colon. It is regulated efficiently by aldosterone levels and recovery from cellular breakdown during haemolysis or tissue damage.
Methods of Control
The K+ in the ECF only represents a very small amount of the total K+ in the body; however its concentration is maintained within very strict parameters. The homeostasis of K+ is managed by three routes:
- Cellular translocation - this is the main method of control; it is an acute response that triggers Potassium movement either into or out of the cells.
- Renal excretion - this method makes up 90% of the chronic response (takes 4-6 hours to respond). It allows fine control and is regulated by aldosterone
- GI excretion - this route makes up the other 10% of the chronic response and becomes significant in cases of renal failure. This response is also influenced by aldosterone
Cellular Translocation
- Vital for rapid control of potassium loads
- Helps control plasma concentration
- Moves potassium into the cell
- Stores potassium in skeletal muscle and liver
- Balances ECF and ICF
- Controlled by insulin and beta2 adrenoreceptors
- Increases the activity of Na+ / K+ ATPases causing sodium efflux and potassium influx
Renal Control
- Potassium ions are reabsorbed and secreted at different points along the nephron
- Active reabsorption of potassium occurs along the proximal tubule (70%) and along the ascending limb of the Loop of Henle (10-20%)
- This results in there only being 10% of the original amount left in the distal tubule
- However net reabsorption / secretion of potassium occurs in the distal tubule and first part of collecting duct
- Depends on bodies need
- Under the influence of aldosterone
- This is where the amount of potassium excreted is determined
- Reabsorption occurs in the final part of the collecting duct
Potassium and Aldosterone
- Aldosterone is the most important regulator of potassium
- It causes increased secretion of potassium
- Increased potassium directly stimulates Aldosterone secretion
- Increases the activity and number of Na+ / K+ ATPase in basolateral membranes of the principal cells in the collecting duct and distal tubule
- Potassium moves into the cells and is then excreted down an electro-chemical gradient
Factors Influencing Potassium Excretion
1.Sodium: High sodium = increased potassium excretion and:
- More sodium into cells
- Increased Na+ / K+ ATPase
- Pumps sodium into peritubular renal interstitium
- The resulting increased cellular uptake of potassium results in it moving down the electrochemical gradient into the nephron
2.Potassium: High potassium = increased potassium excretion which triggers the release of aldosterone.