Diuretic: Difference between revisions

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| Distal convulated tubule || 10% || [[Sodium chloride symporter]] ([[Ion pump]])|| Thiazides
| Distal convulated tubule || 10% || [[Sodium chloride symporter]] ([[Ion pump]])|| Thiazides
|-
|-
| Collecting tubule || 2-5% || [[Sodium channel]] ([[Ion channel]])|| Potassium-sparing diuretics
| Collecting tubule || 2-5% || [[Mineralacorticoid]]s receptors<br>[[Sodium channel]] ([[Ion channel]])|| Potassium-sparing diuretics
|}
|}


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===Potassium-sparing diuretics===
===Potassium-sparing diuretics===
These work in the collecting duct and late distal convoluted tubule.
These work in the collecting duct and late distal convoluted tubule either by inhibiting [[mineralacorticoid]]s receptors or by blocking sodium channels.<ref>{{MeSH|Sodium channel blockers}}</ref><ref name="isbn0-8385-0598-8p483p256">{{cite book |author=Katzung, Bertram G. |title=Basic & Clinical Pharmacology |chapter=Diuretic Agents|publisher=Lange Medical Books/McGraw-Hill |location=New York |year=2001 |pages=256 |isbn=0-8385-0598-8 |oclc= |doi=}}</ref>
 
===Vasopressin antagonists===
Tolvaptan, a [[vasopressin]] antagonist, may be beneficial according to a [[randomized controlled trial]].<ref>Gheorghiade M et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA 2007;297:1332-43. Epub 2007 Mar 25. PMID 17384438</ref><ref>Konstam MA et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA 2007;297:1319-31. Epub 2007 Mar 25. PMID 17384437</ref>  Tolvaptan is a selective [[cell surface receptor]]s V2 antagonist in the distal nephron which causes loss of free water.<ref>Goldsmith SR, Gheorghiade M. Vasopressin antagonism in heart failure. J Am Coll Cardiol. 2005;46:1785-91. PMID 16286160</ref>  Other [[vasopressin]] antagonists act mainly on V1a [[cell surface receptor]]s.
 
===Brain (B-type) natriuretic peptide===
Nesiritide, a brain (B-type) natriuretic peptide, may help patients with decompensated congestive heart failure according to a [[randomized controlled trial]].<ref name="pmid10911006">Colucci WS, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group. N Engl J Med. 2000 Jul 27;343(4):246-53. Erratum in: N Engl J Med 2000 Nov 16;343(20):1504. N Engl J Med 2000;343:896. PMID 10911006</ref> Natriuretic peptide causes diuresis, vasodilitation, and suppression of the [[renin-angiotensin system]] and [[sympathetic nervous system]].<ref name="pmid10911006"/>


==References==
==References==
<references/>
<references/>

Revision as of 23:41, 18 June 2008

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Diuretics are "agents that promote the excretion of urine through their effects on kidney function."[1]

Physiology of sodium reabsorption in the kidney

Physiology of sodium reabsorption in the kidney
Location in nephron Proportion of total sodium reabsorption
accounted for
Membrane transport protein
Ion pump or ion channel
Diuretics that
act at this location
Proximal convulated tubule 40% Sodium-hydrogen antiporter (Ion pump) Carbonic anhydrase inhibitors
Late proximal tubule   Chloride-bicarbonate antiporter (Ion pump) cell
Loop of Henle:
thin descending limb
0% Not applicable Osmotic diuretics
Loop of Henle:
thick ascending limb
('diluting segment')
25% Sodium potassium chloride symporter (Ion pump) Loop diuretics
Distal convulated tubule 10% Sodium chloride symporter (Ion pump) Thiazides
Collecting tubule 2-5% Mineralacorticoids receptors
Sodium channel (Ion channel)
Potassium-sparing diuretics

Classification

Carbonic anhydrase inhibitors

Carbonic anhydrase inhibitors are a "class of compounds that reduces the secretion of h+ ions by the proximal kidney tubule through inhibition of carbonic anhydrases."[2][3]

Osmotic diuretic

Osmotic diuretics are "compounds that increase urine volume by increasing the amount of osmotically active solute in the urine. Osmotic diuretics also increase the osmolarity of plasma."[4]

Loop diuretics

More formally called sodium potassium chloride symporter inhibitors, these are agents that inhibit sodium-potassium-chloride symporters in the thick ascending limb at the junction of the Loop of Henle and distal kidney tubules.[5]

Thiazides

Thiazides are "heterocyclic compounds with sulfur and nitrogen in the ring. This term commonly refers to the benzothiadiazines that inhibit sodium-potassium-chloride symporters."[6]

Potassium-sparing diuretics

These work in the collecting duct and late distal convoluted tubule either by inhibiting mineralacorticoids receptors or by blocking sodium channels.[7][8]

Vasopressin antagonists

Tolvaptan, a vasopressin antagonist, may be beneficial according to a randomized controlled trial.[9][10] Tolvaptan is a selective cell surface receptors V2 antagonist in the distal nephron which causes loss of free water.[11] Other vasopressin antagonists act mainly on V1a cell surface receptors.

Brain (B-type) natriuretic peptide

Nesiritide, a brain (B-type) natriuretic peptide, may help patients with decompensated congestive heart failure according to a randomized controlled trial.[12] Natriuretic peptide causes diuresis, vasodilitation, and suppression of the renin-angiotensin system and sympathetic nervous system.[12]

References

  1. Anonymous (2024), Diuretic (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. Anonymous (2024), Carbonic anhydrase inhibitors (English). Medical Subject Headings. U.S. National Library of Medicine.
  3. Katzung, Bertram G. (2001). “Diuretic Agents”, Basic & Clinical Pharmacology. New York: Lange Medical Books/McGraw-Hill, 249. ISBN 0-8385-0598-8. 
  4. Anonymous (2024), Osmotic diuretics (English). Medical Subject Headings. U.S. National Library of Medicine.
  5. Anonymous (2024), Sodium Potassium Chloride Symporter Inhibitors (English). Medical Subject Headings. U.S. National Library of Medicine.
  6. Anonymous (2024), Thiazides (English). Medical Subject Headings. U.S. National Library of Medicine.
  7. Anonymous (2024), Sodium channel blockers (English). Medical Subject Headings. U.S. National Library of Medicine.
  8. Katzung, Bertram G. (2001). “Diuretic Agents”, Basic & Clinical Pharmacology. New York: Lange Medical Books/McGraw-Hill, 256. ISBN 0-8385-0598-8. 
  9. Gheorghiade M et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA 2007;297:1332-43. Epub 2007 Mar 25. PMID 17384438
  10. Konstam MA et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA 2007;297:1319-31. Epub 2007 Mar 25. PMID 17384437
  11. Goldsmith SR, Gheorghiade M. Vasopressin antagonism in heart failure. J Am Coll Cardiol. 2005;46:1785-91. PMID 16286160
  12. 12.0 12.1 Colucci WS, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. Nesiritide Study Group. N Engl J Med. 2000 Jul 27;343(4):246-53. Erratum in: N Engl J Med 2000 Nov 16;343(20):1504. N Engl J Med 2000;343:896. PMID 10911006