Diuretic: Difference between revisions
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===Potassium-sparing diuretics=== | ===Potassium-sparing diuretics=== | ||
These work in the collecting duct and late distal convoluted tubule either by inhibiting [[mineralacorticoid]]s receptors or by blocking sodium | These work in the collecting duct and late distal convoluted tubule either by inhibiting [[mineralacorticoid]]s receptors or by blocking the epithelial sodium channel.<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> Their ability to treat [[hypertension]] is uncertain.<ref name="pmid20091662">{{cite journal| author=Heran BS, Chen JM, Wang JJ, Wright JM| title=Blood pressure lowering efficacy of potassium-sparing diuretics (that block the epithelial sodium channel) for primary hypertension. | journal=Cochrane Database Syst Rev | year= 2010 | volume= | issue= 1 | pages= CD008167 | pmid=20091662 | ||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=20091662 | doi=10.1002/14651858.CD008167.pub2 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> | |||
===Vasopressin antagonists=== | ===Vasopressin antagonists=== | ||
Revision as of 09:58, 23 February 2010
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% | Carbonic anhydrase Sodium-hydrogen antiporter (Ion pump) |
Carbonic anhydrase inhibitors |
| Late proximal tubule | Chloride-bicarbonate antiporter (Ion pump) | ||
| 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 the epithelial sodium channel.[7][8] Their ability to treat hypertension is uncertain.[9]
Vasopressin antagonists
Tolvaptan, a vasopressin antagonist, may be beneficial according to a randomized controlled trial.[10][11] Tolvaptan is a selective cell surface receptors V2 antagonist in the distal nephron which causes loss of free water.[12] 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.[13] Natriuretic peptide causes diuresis, vasodilitation, and suppression of the renin-angiotensin system and sympathetic nervous system.[13]
Medical uses
Diuretics may be used to treat hypertension, heart failure, and other illnesses.[14] Occasionally high doses or combinations of diuretics are needed.[14][15][16][17]
Adverse effects
Hydrochlorothiazide at doses above 25 mg per day may be associated with sudden cardiac death.[18]
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.
- ↑ Heran BS, Chen JM, Wang JJ, Wright JM (2010). "Blood pressure lowering efficacy of potassium-sparing diuretics (that block the epithelial sodium channel) for primary hypertension.". Cochrane Database Syst Rev (1): CD008167. DOI:10.1002/14651858.CD008167.pub2. PMID 20091662. Research Blogging.
- ↑ 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
- ↑ 13.0 13.1 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
- ↑ 14.0 14.1 Brater DC (August 1998). "Diuretic therapy". N. Engl. J. Med. 339 (6): 387–95. PMID 9691107. [e]
- ↑ Wollam GL, Tarazi RC, Bravo EL, Dustan HP (June 1982). "Diuretic potency of combined hydrochlorothiazide and furosemide therapy in patients with azotemia". Am. J. Med. 72 (6): 929–38. PMID 7046434. [e]
- ↑ Fliser D, Schröter M, Neubeck M, Ritz E (August 1994). "Coadministration of thiazides increases the efficacy of loop diuretics even in patients with advanced renal failure". Kidney Int. 46 (2): 482–8. PMID 7967362. [e]
- ↑ Knauf H, Mutschler E (September 1995). "Diuretic effectiveness of hydrochlorothiazide and furosemide alone and in combination in chronic renal failure". J. Cardiovasc. Pharmacol. 26 (3): 394–400. PMID 8583780. [e]
- ↑ Siscovick DS, Raghunathan TE, Psaty BM, et al (June 1994). "Diuretic therapy for hypertension and the risk of primary cardiac arrest". N. Engl. J. Med. 330 (26): 1852–7. PMID 8196728. [e]