Difference between revisions of "Diuretics Effects on Kidneys - Anatomy & Physiology"
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+ | |linkpage =Urinary System - Anatomy & Physiology | ||
+ | |linktext =URINARY SYSTEM | ||
+ | |maplink = Urinary System (Content Map) - Anatomy & Physiology | ||
+ | |pagetype =Anatomy | ||
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==Introduction== | ==Introduction== | ||
− | + | Duretics are a class of drugs which inhibit the reabsorption of water from the tubules and as a result they increase the volume and therefore water loss in the urine. Each class of diuretic acts on a differant site to achieve this effect. As a result some cause the excretion of sodium (and usually chlorine) along side the water where as others do not. There are several diseases which cause the accumulation of fluid within the various tissues of the body and it is in these cases where diuretics play a role in managing the condition. | |
− | == | + | ==Differant Groups of Diuretics== |
Most diuretics act from within the tubules of the kidney. | Most diuretics act from within the tubules of the kidney. | ||
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===Loop Diuretics=== | ===Loop Diuretics=== | ||
− | Loop diuretics work on the [[ | + | Loop diuretics as the name suggests work on the loop of henle. Specifically on the [[Loop Of Henle - Anatomy & Physiology#Thick ascending limb|thick ascending limb]] where they inhibit the activity of the sodium/potassium/2-chloride symporter. As a result the hypertonicity of the medulla decreases and therefore water unptake from the loop of henle also decreases. Increased amounts of all three ions are lost as a result. |
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− | + | As well as reducing the reuptake of water they also increase renal blood flow via [[The Effects of Nitrous Oxide and Prostaglandins on GFR#Prostaglandins|prostaglandin mediated vasodilation]]. This increases filtration to help lessen fluid retention. | |
− | + | Loop diuretics tend to be bound to plasma protein and therefore are not filtered. They enter the tubule via secretion by the [[Secretion Into The Renal Tubules - Physiology#Primary Active Secretion - Organic Acids and Bases|organic acid transport mechanisms]]. | |
===Thiazides=== | ===Thiazides=== | ||
− | This class of drugs works on the proximal portion of the [[ | + | This class of drugs works on the proximal portion of the [[Distal Tubule - Anatomy & Physiology|distal convoluted tubule]] and inhibits the sodium chloride co-transporter in the apical membrane. As a result they increase the potassium loss - see picture. They are less effective than loop diuretics but are better tolerated. |
− | As with loop diuretics thiazides are excreted into the tubules via [[ | + | As with loop diuretics thiazides are excreted into the tubules via [[Secretion Into The Renal Tubules - Physiology#Primary Active Secretion - Organic Acids and Bases|secretion]]. |
===Potassium Sparing Diuretics=== | ===Potassium Sparing Diuretics=== | ||
− | These diuretics act by blocking the epithelial sodium channel in the [[ | + | These diuretics act by blocking the epithelial sodium channel in the [[Collecting Duct - Anatomy & Physiology|collecting duct]] and therefore reduce sodium and water reabsorption. They do not cause a loss of potassium and thus they get their name as potassium sparing diuretics. |
===Aldosterone Antagonists=== | ===Aldosterone Antagonists=== | ||
− | Without [[Aldosterone]] the cells of the [[ | + | Without [[Aldosterone]] the cells of the [[Collecting Duct - Anatomy & Physiology|collecting duct]] are impermeable to sodium. Therefore if you compete with aldosterone for its receptors you reduce the permeability of the cells to sodium and therefore more sodium and water is excreted. As aldosterone causes the excretion of potassium and calcium from the tubules these two molecules are retained with these drugs. |
===Osmotic Diuretics=== | ===Osmotic Diuretics=== | ||
− | These are compounds which are filtered but not reabsorbed. They increase the osmolarity of the fluid and therefore hold more water in the tubules. However they require intravenous administration. They mainly act on sites freely permeable to water - [[ | + | These are compounds which are filtered but not reabsorbed. They increase the osmolarity of the fluid and therefore hold more water in the tubules. However they require intravenous administration. They mainly act on sites freely permeable to water - [[Proximal Tubule - Anatomy & Physiology |the proximal tubule]], [[Loop Of Henle - Anatomy & Physiology#Thin descending limb|the descending limb of the loop of henle]] and [[Collecting Duct - Anatomy & Physiology |the collecting ducts]]. However they also reduce the sodium uptake as relatively sodium concentration drops in the lumen when they are present. |
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Revision as of 11:55, 20 August 2008
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Introduction
Duretics are a class of drugs which inhibit the reabsorption of water from the tubules and as a result they increase the volume and therefore water loss in the urine. Each class of diuretic acts on a differant site to achieve this effect. As a result some cause the excretion of sodium (and usually chlorine) along side the water where as others do not. There are several diseases which cause the accumulation of fluid within the various tissues of the body and it is in these cases where diuretics play a role in managing the condition.
Differant Groups of Diuretics
Most diuretics act from within the tubules of the kidney.
Loop Diuretics
Loop diuretics as the name suggests work on the loop of henle. Specifically on the thick ascending limb where they inhibit the activity of the sodium/potassium/2-chloride symporter. As a result the hypertonicity of the medulla decreases and therefore water unptake from the loop of henle also decreases. Increased amounts of all three ions are lost as a result.
As well as reducing the reuptake of water they also increase renal blood flow via prostaglandin mediated vasodilation. This increases filtration to help lessen fluid retention.
Loop diuretics tend to be bound to plasma protein and therefore are not filtered. They enter the tubule via secretion by the organic acid transport mechanisms.
Thiazides
This class of drugs works on the proximal portion of the distal convoluted tubule and inhibits the sodium chloride co-transporter in the apical membrane. As a result they increase the potassium loss - see picture. They are less effective than loop diuretics but are better tolerated.
As with loop diuretics thiazides are excreted into the tubules via secretion.
Potassium Sparing Diuretics
These diuretics act by blocking the epithelial sodium channel in the collecting duct and therefore reduce sodium and water reabsorption. They do not cause a loss of potassium and thus they get their name as potassium sparing diuretics.
Aldosterone Antagonists
Without Aldosterone the cells of the collecting duct are impermeable to sodium. Therefore if you compete with aldosterone for its receptors you reduce the permeability of the cells to sodium and therefore more sodium and water is excreted. As aldosterone causes the excretion of potassium and calcium from the tubules these two molecules are retained with these drugs.
Osmotic Diuretics
These are compounds which are filtered but not reabsorbed. They increase the osmolarity of the fluid and therefore hold more water in the tubules. However they require intravenous administration. They mainly act on sites freely permeable to water - the proximal tubule, the descending limb of the loop of henle and the collecting ducts. However they also reduce the sodium uptake as relatively sodium concentration drops in the lumen when they are present.