H2 antagonist - wikipedia H antagonist Ball - and - stick model of cimetidine, the prototypical H - receptor antagonist. H antagonists, sometimes referred to as H2RA and also called H blockers, are a class of medications that block the action of histamine at the histamine H receptors of the parietal cells in the stomach. This decreases the production of stomach acid. H antagonists can be used in the treatment of dyspepsia, peptic ulcers and gastroesophageal reflux disease. They have been surpassed by proton pump inhibitors ( PPIs ) ; the PPI omeprazole was found to be more effective at both healing and alleviating symptoms of ulcers and reflux oesophagitis than the H blockers ranitidine and cimetidine. H antagonists are a type of antihistamine, although in common use the term `` antihistamine '' is often reserved for H antagonists, which relieve allergic reactions. Like the H antagonists, some H antagonists function as inverse agonists rather than receptor antagonists, due to the constitutive activity of these receptors. The prototypical H antagonist, called cimetidine, was developed by Sir James Black at Smith, Kline & French -- now GlaxoSmithKline -- in the mid-to - late 1960s. It was first marketed in 1976 and sold under the trade name Tagamet, which became the first blockbuster drug. The use of quantitative structure - activity relationships ( QSAR ) led to the development of other agents -- starting with ranitidine, first sold as Zantac, which has fewer adverse effects and drug interactions and is more potent. Contents 1 Class members 2 History and development 3 Pharmacology 4 Clinical use 5 Adverse effects 6 Drug interactions 7 References Class members This list may not be exhaustive. cimetidine ranitidine famotidine nizatidine History and development Cimetidine was the prototypical histamine H - receptor antagonist from which later drugs were developed. Cimetidine was the culmination of a project at Smith, Kline & French ( SK&F ; now GlaxoSmithKline ) by James W. Black, C. Robin Ganellin, and others to develop a histamine receptor antagonist that would suppress stomach acid secretion. In 1964, it was known that histamine stimulated the secretion of stomach acid, and also that traditional antihistamines had no effect on acid production. From these facts the SK&F scientists postulated the existence of two different types of histamine receptors. They designated the one acted upon by the traditional antihistamines as H, and the one acted upon by histamine to stimulate the secretion of stomach acid as H. The SK&F team used a classical design process starting from the structure of histamine. Hundreds of modified compounds were synthesised in an effort to develop a model of the then - unknown H receptor. The first breakthrough was N - guanylhistamine, a partial H - receptor antagonist. From this lead, the receptor model was further refined, which eventually led to the development of burimamide, a specific competitive antagonist at the H receptor. Burimamide is 100 times more potent than N - guanylhistamine, proving its efficacy on the H receptor. The potency of burimamide was still too low for oral administration. And efforts on further improvement of the structure, based on the structure modification in the stomach due to the acid dissociation constant of the compound, led to the development of metiamide. Metiamide was an effective agent ; however, it was associated with unacceptable nephrotoxicity and agranulocytosis. It was proposed that the toxicity arose from the thiourea group, and similar guanidine analogues were investigated until the discovery of cimetidine, which would become the first clinically successful H antagonist. Ranitidine ( common brand name Zantac ) was developed by Glaxo ( also now GlaxoSmithKline ), in an effort to match the success of Smith, Kline & French with cimetidine. Ranitidine was also the result of a rational drug design process utilising the by - then - fairly - refined model of the histamine H receptor and quantitative structure - activity relationships ( QSAR ). Glaxo refined the model further by replacing the imidazole - ring of cimetidine with a furan - ring with a nitrogen - containing substituent, and in doing so developed ranitidine. Ranitidine was found to have a far - improved tolerability profile ( i.e. fewer adverse drug reactions ), longer - lasting action, and ten times the activity of cimetidine. Ranitidine was introduced in 1981 and was the world 's biggest - selling prescription drug by 1988. The H - receptor antagonists have since largely been superseded by the even more effective proton pump inhibitors, with omeprazole becoming the biggest - selling drug for many years. Pharmacology The H antagonists are competitive antagonists of histamine at the parietal cell 's H receptor. They suppress the normal secretion of acid by parietal cells and the meal - stimulated secretion of acid. They accomplish this by two mechanisms : Histamine released by ECL cells in the stomach is blocked from binding on parietal cell H receptors, which stimulate acid secretion ; therefore, other substances that promote acid secretion ( such as gastrin and acetylcholine ) have a reduced effect on parietal cells when the H receptors are blocked. Clinical use H - antagonists are used by clinicians in the treatment of acid - related gastrointestinal conditions, including : Peptic ulcer disease ( PUD ) Gastroesophageal reflux disease ( GERD / GORD ) Dyspepsia Prevention of stress ulcer ( a specific indication of ranitidine ) People who suffer from infrequent heartburn may take either antacids or H - receptor antagonists for treatment. The H - antagonists offer several advantages over antacids, including longer duration of action ( 6 -- 10 hours vs 1 -- 2 hours for antacids ), greater efficacy, and ability to be used prophylactically before meals to reduce the chance of heartburn occurring. Proton pump inhibitors, however, are the preferred treatment for erosive esophagitis since they have been shown to promote healing better than H - antagonists. Adverse effects H antagonists are, in general, well - tolerated, except for cimetidine, wherein all of the following adverse drug reactions ( ADRs ) are common. Infrequent ADRs include hypotension. Rare ADRs include : headache, tiredness, dizziness, confusion, diarrhea, constipation, and rash. In addition, gynecomastia occurred in 0.1 % to. 5 % of men treated for nonhypersecretory conditions with cimetidine for 1 month or longer and in about 2 % of men treated for pathologic hypersecretory conditions ; in even fewer men, cimetidine may also cause loss of libido, and impotence, all of which are reversible upon discontinuation. A 31 - study review found that overall risk of pneumonia is about 1 in 4 higher among H antagonist users. Drug interactions Skeletal formula of famotidine. Unlike cimetidine, famotidine has no significant interactions with other drugs. With regard to pharmacokinetics, cimetidine in particular interferes with some of the body 's mechanisms of drug metabolism and elimination through the liver cytochrome P450 ( CYP ) pathway. To be specific, cimetidine is an inhibitor of the P450 enzymes CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4. By reducing the metabolism of drugs through these enzymes, cimetidine may increase their serum concentrations to toxic levels. Many drugs are affected, including warfarin, theophylline, phenytoin, lidocaine, quinidine, propranolol, labetalol, metoprolol, methadone, tricyclic antidepressants, some benzodiazepines, dihydropyridine calcium channel blockers, sulfonylureas, metronidazole, and some recreational drugs such as ethanol and methylenedioxymethamphetamine ( MDMA ). The more recently developed H - receptor antagonists are less likely to alter CYP metabolism. Ranitidine is not as potent a CYP inhibitor as cimetidine, although it still shares several of the latter 's interactions ( such as with warfarin, theophylline, phenytoin, metoprolol, and midazolam ). Famotidine has negligible effect on the CYP system, and appears to have no significant interactions. References Jump up ^ Francis KL Chan ( 21 April 2017 ). `` ASP ( PPI_H2RA ) Study - H2RA Versus PPI for the Prevention of Recurrent UGIB in High - risk Users of Low - dose ASA ''. ClinicalTrials.gov. Retrieved 1 November 2017. Jump up ^ Eriksson S, Långström G, Rikner L, Carlsson R, Naesdal J. Omeprazole and H - receptor antagonists in the acute treatment of duodenal ulcer, gastric ulcer and reflux oesophagitis : a meta - analysis, European Journal of Gastroenterology & Hepatology 1995 ; 7 : 467 -- 475, PMID 7614110. A correction was published in European Journal of Gastroenterology & Hepatology 1996 ; 8 : 192. Jump up ^ Panula P, Chazot PL, Cowart M, et al. ( 2015 ). `` International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors ''. Pharmacological Reviews. 67 ( 3 ) : 601 -- 55. doi : 10.1124 / pr. 114.010249. PMC 4485016. PMID 26084539. Jump up ^ `` Sir James W. Black - Biographical ''. Nobelprize.org. Retrieved 7 April 2015. ^ Jump up to : Rossi S ( Ed. ) ( 2005 ). Australian Medicines Handbook 2005. Adelaide : Australian Medicines Handbook. ISBN 0 - 9578521 - 9 - 3 Jump up ^ Drugs.com `` Cimetidine Side Effects '' Jump up ^ Eom CS, Jeon CY, Lim JW, Cho EG, Park SM, Lee KS ( 2011 ). `` Use of acid - suppressive drugs and risk of pneumonia : a systematic review and meta - analysis ''. CMAJ. 183 ( 3 ) : 310 -- 9. doi : 10.1503 / cmaj. 092129. PMC 3042441. PMID 21173070. ( adjusted odds ratio ( OR ) 1.22 ) ^ Jump up to : Humphries TJ, Merritt GJ ( August 1999 ). `` Review article : drug interactions with agents used to treat acid - related diseases ''. Alimentary Pharmacology & Therapeutics. 13 Suppl 3 : 18 -- 26. doi : 10.1046 / j. 1365 - 2036.1999. 00021. x. PMID 10491725. Jump up ^ Kirch W, Hoensch H, Janisch HD ( 1984 ). `` Interactions and non-interactions with ranitidine ''. Clinical Pharmacokinetics. 9 ( 6 ) : 493 -- 510. doi : 10.2165 / 00003088 - 198409060 - 00002. PMID 6096071. This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. ( December 2013 ) Pharmacology : major drug groups Gastrointestinal tract / metabolism ( A ) stomach acid Antacids H antagonists Proton pump inhibitors Antiemetics Laxatives Antidiarrhoeals / Antipropulsives Anti-obesity drugs Anti-diabetics Vitamins Dietary minerals Blood and blood forming organs ( B ) Antithrombotics Antiplatelets Anticoagulants Thrombolytics / fibrinolytics Antihemorrhagics Platelets Coagulants Antifibrinolytics Cardiovascular system ( C ) cardiac therapy / antianginals Cardiac glycosides Antiarrhythmics Cardiac stimulants Antihypertensives Diuretics Vasodilators Beta blockers Calcium channel blockers renin -- angiotensin system ACE inhibitors Angiotensin II receptor antagonists Renin inhibitors Antihyperlipidemics Statins Fibrates Bile acid sequestrants Skin ( D ) Emollients Cicatrizants Antipruritics Antipsoriatics Medicated dressings Genitourinary system ( G ) Hormonal contraception Fertility agents SERMs Sex hormones Endocrine system ( H ) Hypothalamic -- pituitary hormones Corticosteroids Glucocorticoids Mineralocorticoids Sex hormones Thyroid hormones / Antithyroid agents Infections and infestations ( J, P, QI ) Antimicrobials : Antibacterials ( Antimycobacterials ) Antifungals Antivirals Antiparasitics Antiprotozoals Anthelmintics Ectoparasiticides IVIG Vaccines Malignant disease ( L01 -- L02 ) Anticancer agents Antimetabolites Alkylating Spindle poisons Antineoplastic Topoisomerase inhibitors Immune disease ( L03 -- L04 ) Immunomodulators Immunostimulants Immunosuppressants Muscles, bones, and joints ( M ) Anabolic steroids Anti-inflammatories NSAIDs Antirheumatics Corticosteroids Muscle relaxants Bisphosphonates Brain and nervous system ( N ) Analgesics Anesthetics General Local Anorectics Anti-ADHD agents Antiaddictives Anticonvulsants Antidementia agents Antidepressants Antimigraine agents Antiparkinson agents Antipsychotics Anxiolytics Depressants Entactogens Entheogens Euphoriants Hallucinogens Psychedelics Dissociatives Deliriants Hypnotics / Sedatives Mood Stabilizers Neuroprotectives Nootropics Neurotoxins Orexigenics Serenics Stimulants Wakefulness - promoting agents Respiratory system ( R ) Decongestants Bronchodilators Cough medicines H antagonists Sensory organs ( S ) Ophthalmologicals Otologicals Other ATC ( V ) Antidotes Contrast media Radiopharmaceuticals Dressings Senotherapeutics Pharmacomodulation Types Enzyme : Inducer Inhibitor Ion channel : Opener Blocker Receptor : Agonist Partial agonist Antagonist Inverse agonist Positive allosteric modulator ( PAM ) Negative allosteric modulator ( NAM ) Transporter ( Reuptake vs Efflux ) : Enhancer ( RE ) Inhibitor ( RI ) Releaser ( RA ) Miscellaneous : Precursor Cofactor Classes Enzyme see Enzyme inhibition Ion channel Calcium channel blocker ( CCB ) Potassium channel blocker ( PCB ) Sodium channel blocker ( SCB ) Potassium channel opener ( PCO ) Receptor & transporter BA / M Adrenergic Adrenergic receptor agonist ( α β ( 1 2 ) ) Adrenergic receptor antagonist ( α ( 1 2 ) β ) Norepinephrine reuptake inhibitor ( NRI ) Dopaminergic Dopamine receptor agonist Dopamine receptor antagonist Dopamine reuptake inhibitor ( DRI ) Histaminergic Histamine receptor agonist Histamine receptor antagonist ( H H ) Serotonergic Serotonin receptor agonist Serotonin receptor antagonist ( 5 - HT ) Serotonin reuptake inhibitor ( SRI ) AA GABAergic GABA receptor agonist GABA receptor antagonist GABA reuptake inhibitor ( GRI ) Glutamatergic Glutamate receptor agonist ( AMPA ) Glutamate receptor antagonist ( NMDA ) Glutamate reuptake inhibitor Cholinergic Acetylcholine receptor agonist ( Muscarinic Nicotinic ) Acetylcholine receptor antagonist ( Muscarinic Nicotinic ( Ganglionic Muscular ) ) Cannabinoidergic Cannabinoid receptor agonist Cannabinoid receptor antagonist Endocannabinoid enhancer ( eCBE ) Endocannabinoid reuptake inhibitor ( eCBRI ) Opioidergic Opioid modulator Opioid receptor agonist Opioid receptor antagonist Enkephalinase inhibitor Other Adenosine reuptake inhibitor ( AdoRI ) Angiotensin II receptor antagonist Endothelin receptor antagonist NK receptor antagonist Vasopressin receptor antagonist Miscellaneous Cofactor ( see Enzyme cofactors ) Precursor ( see Amino acids ) Drugs for peptic ulcer and GERD / GORD ( A02B ) H antagonists ( `` - tidine '' ) Cimetidine Famotidine Lafutidine Lavoltidine ( loxtidine ) Niperotidine Nizatidine Ranitidine Roxatidine Prostaglandins ( E ) / analogues ( `` - prost - '' ) Misoprostol Enprostil Proton - pump inhibitors ( `` - prazole '' ) Azeloprazole Dexlansoprazole Esomeprazole Ilaprazole Lansoprazole Omeprazole Pantoprazole Picoprazole Rabeprazole Tenatoprazole Timoprazole Potassium - competitive acid blockers ( `` - prazan '' ) Linaprazan Revaprazan Soraprazan Vonoprazan Others Aceglutamide aluminum Acetoxolone Alginic acid Arbaclofen placarbil Bismuth subcitrate Carbenoxolone Cetraxate Gefarnate Lesogaberan Pirenzepine Proglumide Rebamipide Sucralfate Sulglicotide Telenzepine Teprenone Troxipide Zinc L - carnosine Zolimidine Combinations Bismuth subcitrate / metronidazole / tetracycline See also : Helicobacter pylori eradication protocols Histamine receptor modulators Agonists : 2 - Pyridylethylamine Betahistine Histamine HTMT L - Histidine UR - AK49 Antagonists : First - generation : 4 - Methyldiphenhydramine Alimemazine Antazoline Azatadine Bamipine Benzatropine ( benztropine ) Bepotastine Bromazine Brompheniramine Buclizine Captodiame Carbinoxamine Chlorcyclizine Chloropyramine Chlorothen Chlorphenamine Chlorphenoxamine Cinnarizine Clemastine Clobenzepam Clocinizine Cloperastine Cyclizine Cyproheptadine Dacemazine Decloxizine Deptropine Dexbrompheniramine Dexchlorpheniramine Dimenhydrinate Dimetindene Diphenhydramine Diphenylpyraline Doxylamine Embramine Etodroxizine Etybenzatropine ( ethylbenztropine ) Etymemazine Fenethazine Flunarizine Histapyrrodine Homochlorcyclizine Hydroxyethylpromethazine Hydroxyzine Isopromethazine Isothipendyl Meclozine Medrylamine Mepyramine ( pyrilamine ) Mequitazine Methafurylene Methapyrilene Methdilazine Moxastine Orphenadrine Oxatomide Oxomemazine Perlapine Phenindamine Pheniramine Phenyltoloxamine Pimethixene Piperoxan Pipoxizine Promethazine Propiomazine Pyrrobutamine Talastine Thenalidine Thenyldiamine Thiazinamium Thonzylamine Tolpropamine Tripelennamine Triprolidine Second / third - generation : Acrivastine Alinastine Astemizole Azelastine Bamirastine Barmastine Bepiastine Bepotastine Bilastine Cabastinen Carebastine Cetirizine Clemastine Clemizole Clobenztropine Desloratadine Dorastine Ebastine Efletirizine Emedastine Epinastine Fexofenadine Flezelastine Ketotifen Latrepirdine Levocabastine Levocetirizine Linetastine Loratadine Mapinastine Mebhydrolin Mizolastine Moxastine Noberastine Octastine Olopatadine Perastine Pibaxizine Piclopastine Quifenadine ( phencarol ) Rocastine Rupatadine Setastine Sequifenadine ( bicarphen ) Talastine Temelastine Terfenadine Vapitadine Zepastine Others : Atypical antipsychotics ( e.g., aripiprazole, asenapine, brexpiprazole, clozapine, iloperidone, olanzapine, paliperidone, quetiapine, risperidone, RP - 5063, ziprasidone, zotepine ) Phenylpiperazine antidepressants ( e.g., hydroxynefazodone, nefazodone, trazodone, triazoledione ) Tetracyclic antidepressants ( e.g., amoxapine, loxapine, maprotiline, mianserin, mirtazapine, oxaprotiline ) Tricyclic antidepressants ( e.g., amitriptyline, butriptyline, clomipramine, desipramine, dosulepin ( dothiepin ), doxepin, imipramine, iprindole, lofepramine, nortriptyline, protriptyline, trimipramine ) Typical antipsychotics ( e.g., chlorpromazine, flupenthixol, fluphenazine, loxapine, perphenazine, prochlorperazine, thioridazine, thiothixene ) Unknown / unsorted : Azanator Belarizine Elbanizine Flotrenizine GSK1004723 Napactadine Tagorizine Trelnarizine Trenizine Agonists : Amthamine Betazole Dimaprit Histamine HTMT Impromidine L - Histidine UR - AK49 Antagonists : Bisfentidine Burimamide Cimetidine Dalcotidine Donetidine Ebrotidine Etintidine Famotidine Isolamtidine Lafutidine Lamtidine Lavoltidine ( loxtidine ) Lupitidine Metiamide Mifentidine Niperotidine Nizatidine Osutidine Oxmetidine Pibutidine Quisultazine ( quisultidine ) Ramixotidine Ranitidine Roxatidine Sufotidine Tiotidine Tuvatidine Venritidine Xaltidine Zolantidine Agonists : α - Methylhistamine Cipralisant Histamine Imetit Immepip Immethridine L - Histidine Methimepip Proxyfan Antagonists : A-349,821 A-423,579 ABT - 239 ABT - 652 AZD5213 Bavisant Betahistine Burimamide Ciproxifan Clobenpropit Conessine Enerisant GSK - 189,254 Impentamine Iodophenpropit Irdabisant JNJ - 5207852 MK - 0249 NNC 38 - 1049 PF - 03654746 Pitolisant SCH - 79687 Thioperamide VUF - 5681 Agonists : 4 - Methylhistamine α - Methylhistamine Histamine L - Histidine OUP - 16 VUF - 8430 Antagonists : JNJ - 7777120 Mianserin Seliforant Thioperamide Toreforant VUF - 6002 See also : Receptor / signaling modulators Monoamine metabolism modulators Monoamine reuptake inhibitors Retrieved from `` https://en.wikipedia.org/w/index.php?title=H2_antagonist&oldid=848388897 '' Categories : H2 receptor antagonists Hidden categories : All articles with unsourced statements Articles with unsourced statements from March 2015 Articles needing additional references from December 2013 All articles needing additional references Talk Contents About Wikipedia Català Deutsch Español Français Gaeilge Hrvatski Bahasa Indonesia Italiano Nederlands 日本 語 Polski Português Русский Slovenščina Српски / srpski Srpskohrvatski / српскохрватски Svenska ไทย Türkçe Українська 中文 13 more Edit links This page was last edited on 1 July 2018, at 16 : 29 ( UTC ). Text is available under the Creative Commons Attribution - ShareAlike License ; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia ® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization. About Wikipedia

Question: what does a histamine 2 receptor antagonist do
Answer: block the action of histamine at the histamine H2 receptors of the parietal cells in the stomach