Which of the Following Can Act as a Diuretic

Substance that promotes the product of urine

Drug form

Furosemide 125mg vials for intravenous application

Class identifiers
Apply Forced diuresis, hypertension
ATC lawmaking C03
External links
MeSH D004232
In Wikidata

() is whatsoever substance that promotes diuresis, the increased product of urine. This includes forced diuresis. A diuretic tablet is sometimes colloquially called a
water tablet. At that place are several categories of diuretics. All diuretics increment the excretion of h2o from the body, through the kidneys. There be several classes of diuretic, and each works in a distinct manner. Alternatively, an antidiuretic, such as vasopressin (antidiuretic hormone), is an agent or drug which reduces the excretion of water in urine.

Medical uses


In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, flu, water poisoning, and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion of substances such as aspirin in cases of overdose or poisoning. Diuretics are sometimes abused by people with an eating disorder, particularly people with bulimia nervosa, with the goal of losing weight.

The antihypertensive deportment of some diuretics (thiazides and loop diuretics in item) are contained of their diuretic issue.[1]
That is, the reduction in blood force per unit area is not due to decreased claret volume resulting from increased urine production, but occurs through other mechanisms and at lower doses than that required to produce diuresis. Indapamide was specifically designed with this in listen, and has a larger therapeutic window for hypertension (without pronounced diuresis) than most other diuretics.



High-ceiling/loop diuretics


High-ceiling diuretics may cause a substantial diuresis – up to xx%[three]
of the filtered load of NaCl (salt) and h2o. This is big in comparing to normal renal sodium reabsorption which leaves only about 0.four% of filtered sodium in the urine. Loop diuretics have this ability, and are therefore often synonymous with high-ceiling diuretics. Loop diuretics, such as furosemide, inhibit the body’s power to reabsorb sodium at the ascending loop in the nephron, which leads to an excretion of water in the urine, whereas water normally follows sodium dorsum into the extracellular fluid. Other examples of high-ceiling loop diuretics include ethacrynic acid and torasemide.[
citation needed



Thiazide-blazon diuretics such equally hydrochlorothiazide act on the distal convoluted tubule and inhibit the sodium-chloride symporter leading to a memory of water in the urine, as water commonly follows penetrating solutes. Frequent urination is due to the increased loss of water that has not been retained from the torso every bit a result of a concomitant human relationship with sodium loss from the convoluted tubule. The short-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing claret pressure. On the other hand, the long-term effect is due to an unknown vasodilator effect that decreases claret pressure by decreasing resistance.[4]

Carbonic anhydrase inhibitors


Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase which is found in the proximal convoluted tubule. This results in several furnishings including bicarbonate accumulation in the urine and decreased sodium absorption. Drugs in this class include acetazolamide and methazolamide.

Potassium-sparing diuretics


These are diuretics which practise non promote the secretion of potassium into the urine; thus, potassium is retained and non lost as much as with other diuretics. The term “potassium-sparing” refers to an issue rather than a mechanism or location; even so, the term almost e’er refers to two specific classes that take their upshot at similar locations:

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  • Aldosterone antagonists: spironolactone, which is a competitive antagonist of aldosterone. Aldosterone usually adds sodium channels in the main cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. Similar agents are eplerenone and potassium canreonate.
  • Epithelial sodium aqueduct blockers: amiloride and triamterene.

Calcium-sparing diuretics


The term “calcium-sparing diuretic” is sometimes used to identify agents that event in a relatively low rate of excretion of calcium.[5]

The reduced concentration of calcium in the urine can lead to an increased rate of calcium in serum. The sparing outcome on calcium can be benign in hypocalcemia, or unwanted in hypercalcemia.

The thiazides and potassium-sparing diuretics are considered to exist calcium-sparing diuretics.[6]

  • The thiazides cause a net
    in calcium lost in urine.[seven]
  • The potassium-sparing diuretics crusade a net
    in calcium lost in urine, but the increase is
    much smaller
    than the increase associated with other diuretic classes.[seven]

Past dissimilarity, loop diuretics promote a pregnant increase in calcium excretion.[eight]
This can increase risk of reduced os density.[ix]

Osmotic diuretics


Osmotic diuretics (e.thousand. mannitol) are substances that increase osmolarity but have express tubular epithelial cell permeability. They piece of work primarily by expanding extracellular fluid and plasma book, therefore increasing blood flow to the kidney, particularly the peritubular capillaries. This reduces medullary osmolality and thus impairs the concentration of urine in the loop of Henle (which unremarkably uses the high osmotic and solute gradient to ship solutes and water). Farther, the express tubular epithelial cell permeability increases osmolality and thus h2o retention in the filtrate.[10]

Information technology was previously believed that the master mechanism of osmotic diuretics such as mannitol is that they are filtered in the glomerulus, but cannot exist reabsorbed. Thus their presence leads to an increment in the osmolarity of the filtrate and to maintain osmotic residual, water is retained in the urine.

Glucose, like mannitol, is a carbohydrate that tin can behave as an osmotic diuretic. Unlike mannitol, glucose is commonly found in the blood. However, in certain atmospheric condition, such as diabetes mellitus, the concentration of glucose in the claret (hyperglycemia) exceeds the maximum reabsorption capacity of the kidney. When this happens, glucose remains in the filtrate, leading to the osmotic retention of water in the urine. Glucosuria causes a loss of hypotonic water and Na+, leading to a hypertonic state with signs of book depletion, such as dry mucosa, hypotension, tachycardia, and decreased turgor of the skin. Employ of some drugs, especially stimulants, may also increase claret glucose and thus increase urination.[
citation needed

Low-ceiling diuretics


The term “depression-ceiling diuretic” is used to point a diuretic has a chop-chop flattening dose upshot curve (in contrast to “high-ceiling”, where the relationship is shut to linear). Sure classes of diuretic are in this category, such every bit the thiazides.[11]

Machinery of action


Diuretics are tools of considerable therapeutic importance. First, they effectively reduce blood force per unit area. Loop and thiazide diuretics are secreted from the proximal tubule via the organic anion transporter-1 and exert their diuretic activeness by binding to the Na(+)-1000(+)-2Cl(-) co-transporter type ii in the thick ascending limb and the Na(+)-Cl(-) co-transporter in the distal convoluted tubule, respectively.[12]
Nomenclature of common diuretics and their mechanisms of action.

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Examples Mechanism Location (numbered in altitude along nephron)
ethanol (alcohol), water Inhibits vasopressin secretion
Acidifying salts calcium chloride, ammonium chloride 1.
Arginine vasopressin
receptor 2 antagonists
amphotericin B, lithium[13]
Inhibits vasopressin’s action 5. collecting duct
Selective vasopressin V2 adversary (sometimes called aquaretics) tolvaptan,[xv]
Competitive vasopressin antagonism leads to decreased number of aquaporin channels in the apical membrane of the renal collecting ducts in kidneys, causing decreased water reabsorption. This causes an increase in renal free water excretion (aquaresis), an increase in serum sodium concentration, a decrease in urine osmolality, and an increase in urine output.[xvi] 5. collecting duct
Na-H exchanger antagonists dopamine[17] Promotes Na+
2. proximal tubule[17]
Carbonic anhydrase inhibitors acetazolamide,[17]
Inhibits H+
secretion, resultant promotion of Na+
and K+
two. proximal tubule
Loop diuretics bumetanide,[17]
ethacrynic acid,[17]
Inhibits the Na-K-2Cl symporter iii. medullary thick ascending limb
Osmotic diuretics glucose (especially in uncontrolled diabetes), mannitol Promotes osmotic diuresis 2. proximal tubule, descending limb
Potassium-sparing diuretics amiloride, spironolactone, eplerenone, triamterene, potassium canrenoate. Inhibition of Na+/Thousand+ exchanger: Spironolactone inhibits aldosterone activity, Amiloride inhibits epithelial sodium channels[17] five. cortical collecting ducts
Thiazides bendroflumethiazide, hydrochlorothiazide Inhibits reabsorption by Na+/Cl
4. distal convoluted tubules
Xanthines caffeine, theophylline, theobromine Inhibits reabsorption of Na+, increase glomerular filtration rate 1. tubules

Chemically, diuretics are a diverse group of compounds that either stimulate or inhibit various hormones that naturally occur in the body to regulate urine production by the kidneys.

Equally a diuretic is whatsoever substance that promotes the production of urine, aquaretics that cause the excretion of free water are a sub-course. This includes all the hypotonic aqueous preparations, including pure water, black and green teas, and teas prepared from herbal medications. Any given herbal medication volition include a vast range of plant-derived compounds, some of which volition be active drugs that may also take independent diuretic action.

Adverse effects


The main adverse effects of diuretics are hypovolemia, hypokalemia, hyperkalemia, hyponatremia, metabolic alkalosis, metabolic acidosis, and hyperuricemia.[17]

Adverse effect Diuretics Symptoms
  • loop diuretics[17]
  • thiazides[17]
  • lassitude[17]
  • thirst[17]
  • muscle cramps[17]
  • hypotension[17]
  • acetazolamides[17]
  • loop diuretics[17]
  • thiazides[17]
  • muscle weakness[17]
  • paralysis[17]
  • arrhythmia[17]
  • amilorides[17]
  • triamterenes[17]
  • spironolactone[17]
  • arrhythmia[17]
  • muscle cramps[17]
  • paralysis[17]
  • thiazides[17]
  • furosemides[17]
  • CNS symptoms[17]
    • coma[17]
metabolic alkalosis
  • loop diuretics[17]
  • thiazides[17]
  • arrhythmia[17]
  • CNS symptoms[17]
metabolic acidosis
  • acetazolamides[17]
  • amilorides[17]
  • triamterene[17]
  • Kussmaul respirations[17]
  • musculus weakness
  • neurological symptoms[17]
    • lethargy
    • coma
    • seizures
    • stupor
  • thiazides[17]
  • gout
  • tissue calcification[17]
  • fatigue
  • depression
  • confusion
  • anorexia
  • nausea
  • vomiting
  • constipation
  • pancreatitis
  • increased urination
  • loop diuretics[17]
  • thiazides[17]
  • gout[17]

Abuse in sports


A common awarding of diuretics is for the purposes of invalidating drug tests.[eighteen]
Diuretics increase the urine volume and dilute doping agents and their metabolites. Some other employ is to apace lose weight to meet a weight category in sports like boxing and wrestling.[19]

See too


  • Antidiuretic
  • Laxative
  • Diuresis
  • Hydration
  • Water poisoning
  • Dehydration



  1. ^

    Shah, Shaukat; Khatri, Ibrahim; Freis, Edward D. (1978). “Machinery of antihypertensive issue of thiazide diuretics”.
    American Heart Journal.
    (5): 611–618. doi:10.1016/0002-8703(78)90303-4. PMID 637001.

  2. ^

    Ballew JR, Fink GD (September 2001). “Characterization of the antihypertensive effect of a thiazide diuretic in angiotensin II-induced hypertension”.
    Journal of Hypertension.
    (9): 1601–half-dozen. doi:10.1097/00004872-200109000-00012. PMID 11564980. S2CID 8531997.

  3. ^

    Drug Monitor – Diuretics Archived January 17, 2008, at the Wayback Machine

  4. ^

    Julio D. Duarte; Rhonda M. Cooper-DeHoff (April 1, 2011). “Mechanisms for blood pressure lowering and metabolic effects of thiazide and thiazide-like diuretics”.
    Expert Review of Cardiovascular Therapy.
    (half dozen): 793–802. doi:ten.1586/erc.10.27. PMC2904515. PMID 20528637.

  5. ^

    Shankaran South, Liang KC, Ilagan N, Fleischmann L (Apr 1995). “Mineral excretion following furosemide compared with bumetanide therapy in premature infants”.
    Pediatr. Nephrol.
    (2): 159–62. doi:10.1007/BF00860731. PMID 7794709. S2CID 21202583.

  6. ^

    Bakhireva LN, Barrett-Connor E, Kritz-Silverstein D, Morton DJ (June 2004). “Modifiable predictors of bone loss in older men: a prospective study”.
    Am J Prev Med.
    (5): 436–42. doi:10.1016/j.amepre.2004.02.013. PMID 15165661.

  7. ^



    Champe, Pamela C.; Richard Hubbard Howland; Mary Julia Mycek; Harvey, Richard P. (2006).
    Pharmacology. Philadelphia: Lippincott William & Wilkins. p. 269. ISBN978-0-7817-4118-7.

  8. ^

    Rejnmark L, Vestergaard P, Pedersen AR, Heickendorff L, Andreasen F, Mosekilde Fifty (Jan 2003). “Dose-effect relations of loop- and thiazide-diuretics on calcium homeostasis: a randomized, double-blinded Latin-foursquare multiple cross-over written report in postmenopausal osteopenic women”.
    Eur. J. Clin. Invest.
    (1): 41–50. doi:10.1046/j.1365-2362.2003.01103.x. PMID 12492451. S2CID 36030615.

  9. ^

    Rejnmark L, Vestergaard P, Heickendorff L, Andreasen F, Mosekilde L (January 2006). “Loop diuretics increment bone turnover and decrease BMD in osteopenic postmenopausal women: results from a randomized controlled study with bumetanide”.
    J. Bone Miner. Res.
    (1): 163–lxx. doi:10.1359/JBMR.051003. PMID 16355285. S2CID 41216704.

  10. ^

    Du, Xiaoping. Diuretics Archived April vii, 2006, at the Wayback Automobile. Department of Pharmacology, University of Illinois at Chicago.

  11. ^

    Mutschler, Ernst (1995).
    Drug actions: basic principles and therapeutic aspects. Stuttgart, German: Medpharm Scientific Pub. p. 460. ISBN978-0-8493-7774-vii.

  12. ^

    Ali SS, Sharma PK, Garg VK, Singh AK, Mondal SC (Apr 2012). “The target-specific transporter and current condition of diuretics every bit antihypertensive”.
    Fundam Clin Pharmacol.
    (two): 175–nine. doi:10.1111/j.1472-8206.2011.01012.10. PMID 22145583. S2CID 43171023.

  13. ^

    Ajay K. Singh; Gordon H. Williams (12 January 2009).
    Textbook of Nephro-Endocrinology. Academic Press. pp. 250–251. ISBN978-0-08-092046-seven.

  14. ^

    Fifty. Kovács; B. Lichardus (6 December 2012).
    Vasopressin: Disturbed Secretion and Its Effects. Springer Science & Business Media. pp. 179–180. ISBN978-94-009-0449-1.

  15. ^

    Schrier, Robert Westward.; Gross, Peter; Gheorghiade, Mihai; Berl, Tomas; Verbalis, Joseph G.; Czerwiec, Frank Due south.; Orlandi, Cesare (2006-11-16). “Tolvaptan, a Selective Oral Vasopressin V2-Receptor Antagonist, for Hyponatremia”.
    New England Journal of Medicine.
    (20): 2099–2112. doi:10.1056/NEJMoa065181. hdl:2437/157922. ISSN 0028-4793. PMID 17105757.

  16. ^

    Reilly, Timothy; Chavez, Benjamin (2009-10-01). “Tolvaptan (samsca) for hyponatremia: is it worth its salt?”.
    Pharmacy and Therapeutics.
    (x): 543–547. PMC2799145.

  17. ^













































    Boron, Walter F. (2004).
    Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. p. 875. ISBN978-ane-4160-2328-9.

  18. ^

    Bahrke, Michael (2002).
    Performance-Enhancing Substances in Sport and Do.

  19. ^

    Agence France Presse (2012-07-17). “UCI announces agin analytical finding for Frank Schleck”. VeloNews. Retrieved

  20. ^

    Cadwallader AB, de la Torre X, Tieri A, Botrè F (September 2010). “The abuse of diuretics as performance-enhancing drugs and masking agents in sport doping: pharmacology, toxicology and analysis”.
    British Journal of Pharmacology.
    (1): 1–16. doi:10.1111/j.1476-5381.2010.00789.ten. PMC2962812. PMID 20718736.

External links


  • Diagram at cvpharmacology.com
  • “Caffeine and Electrolyte Imbalance” by Dana George August 23, 2011
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Which of the Following Can Act as a Diuretic

Source: https://en.wikipedia.org/wiki/Diuretic

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