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 | ||
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| 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 22:41, 18 June 2008
Diuretics are "agents that promote the excretion of urine through their effects on kidney function."[1]
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
- ↑ Anonymous (2024), Diuretic (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Carbonic anhydrase inhibitors (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Katzung, Bertram G. (2001). “Diuretic Agents”, Basic & Clinical Pharmacology. New York: Lange Medical Books/McGraw-Hill, 249. ISBN 0-8385-0598-8.
- ↑ Anonymous (2024), Osmotic diuretics (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Sodium Potassium Chloride Symporter Inhibitors (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Thiazides (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Anonymous (2024), Sodium channel blockers (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Katzung, Bertram G. (2001). “Diuretic Agents”, Basic & Clinical Pharmacology. New York: Lange Medical Books/McGraw-Hill, 256. ISBN 0-8385-0598-8.
- ↑ 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
- ↑ 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
- ↑ Goldsmith SR, Gheorghiade M. Vasopressin antagonism in heart failure. J Am Coll Cardiol. 2005;46:1785-91. PMID 16286160
- ↑ 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