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20-September-2008 09:55:56 - Nicotine This article is about the chemical compound. For other uses, see Nicotine disambiguation. Nicotine Systematic IUPAC name S-3-1-Methyl-2-pyrrolidinylpyridine Identifiers CAS number 54-11-5 ATC code N07BA01 PubChem 942 Chemical data Formula C10H14N2 Mol. mass 162.26 g/mol SMILES eMolecules PubChem Physical data Density 1.01 g/cm³ Melt. point -79 °C -110 °F Boiling point 247 °C 477 °F Pharmacokinetic data Bioavailability ? Metabolism ? Half life 2 hours Excretion ? Therapeutic considerations Pregnancy cat. DUS Legal status UnscheduledAU ?UK Dependence Liability Medium to high Routes Smoked as tobacco, Insufflated as snuff, Chewed Nicotine is an alkaloid found in the nightshade family of plants Solanaceae1, predominantly in tobacco, and in lower quantities in tomato, potato, eggplant aubergine, and green pepper. Nicotine can also be found, along with cocaine, in the leaves of the coca plant. Nicotine has been found to constitute approximately 0.6-3.0% of dry weight of tobacco,2 with biosynthesis taking place in the roots, and accumulating in the leaves. It functions as an antiherbivore chemical, being a potent neurotoxin with particular specificity to insects; therefore nicotine was widely used as an insecticide in the past, and currently nicotine analogs such as imidacloprid continue to be widely used. In low concentrations an average cigarette yields about 1 mg of absorbed nicotine,an electronic cigarette may or may not contain nicotine,such as Ruyan v83, the substance acts as a stimulant in mammals and is one of the main factors responsible for the dependence-forming properties of tobacco smoking. According to the American Heart Association, Nicotine addiction has historically been one of the hardest addictions to break. The pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.4 Contents 1 History and name 2 Chemistry 3 Pharmacology 3.1 Pharmacokinetics 3.2 Pharmacodynamics 3.2.1 In adrenal medulla 3.2.2 In CNS 4 Psychoactive effects 5 Dependence 6 Toxicology 7 Nicotine and oxidative stress 8 Link to circulatory disease 9 Therapeutic uses 10 See also 11 External links 12 References 13 Further reading History and name Nicotine is named after the tobacco plant Nicotiana tabacum, which in turn is named after Jean Nicot, French ambassador in Portugal, who sent tobacco and seeds from Brazil to Paris in 1560 and promoted their medicinal use. Nicotine was first isolated from the tobacco plant in 1828 by German chemists Posselt Reimann.citation needed Its chemical empirical formula was described by Melsens in 1843,5, its structre was discovered by Adolf Pinner in 1893, and it was first synthesized by A. Pictet and Crepieux in 1904.citation needed - Chemistry Nicotine is a hygroscopic, oily liquid that is miscible with water in its base form. As a nitrogenous base, nicotine forms salts with acids that are usually solid and water soluble. Nicotine easily penetrates the skin. As shown by the physical data, free base nicotine will burn at a temperature below its boiling point, and its vapors will combust at 308K 35°C or 95°F in air despite a low vapor pressure. Because of this, most of the nicotine is burned when a cigarette is smoked; however, enough is inhaled to provide the desired effects. Pharmacology Pharmacokinetics As nicotine enters the body, it is distributed quickly through the bloodstream and can cross the blood-brain barrier. On average it takes about seven seconds for the substance to reach the brain when inhaled. The half life of nicotine in the body is around two hours.6 The amount of nicotine inhaled with tobacco smoke is a fraction of the amount contained in the tobacco leaves. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. For chewing tobacco, dipping tobacco and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is metabolized in the liver by cytochrome P450 enzymes mostly CYP2A6, and also by CYP2B6. A major metabolite is cotinine. Pharmacodynamics Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS type nicotinic receptor. The former is present e.g. in the adrenal medulla and the latter in the CNS. In small concentrations it increases the activity of these receptors. In adrenal medulla By binding to ganglion type nicotinic receptors in the adrenal medulla nicotine increases flow of adrenaline epinephrine, a stimulating hormone. By binding to the receptors, it causes cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine and norepinephrine into the bloodstream. The release of adrenaline causes an increase in heart rate, blood pressure and respiration, as well as higher blood glucose levels7 Cotinine is a byproduct of the metabolism of nicotine which remains in the blood for up to 48 hours and can be used as an indicator of a person's exposure to smoke. In CNS By binding to CNS type nicotinic receptors, nicotine increases dopamine levels in the reward circuits of the brain. In this way, it activates the reward system and generates feelings of pleasure. Furthermore, nicotine activates the sympathetic nervous system,8 acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine and norepinephrine into the bloodstream. Studies have shown that other ingredients in inhaled tobacco smoke as opposed to pure nicotine inhibit the production of monoamine oxidase MAO,9 an enzyme responsible for breaking down monoaminergic neurotransmitters, such as dopamine, in the brain. The compounds responsible for this effect are beta-carboline alkaloids such as harmane and norharmane. Psychoactive effects Nicotine's mood-altering effects are different by report. First causing a release of glucose from the liver and epinephrine adrenaline from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, calmness, and alertness.10 It is even reported to produce a mildly euphoric state. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.1112 When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers including acetylcholine, norepinephrine, epinephrine, vasopressin, arginine, dopamine, and beta-endorphincitation needed. This results in enhanced pleasurecitation needed, decreased anxietycitation needed, and a state of alert relaxationcitation needed. Nicotine enhances concentrationcitation needed and learningcitation needed due to the increase of acetylcholine. It also enhances alertness due to the increases of acetylcholine and norepinephrine. Arousal is increased by the increase of norepinephrine. Pain is reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also sensitises brain reward systems.13 Most cigarettes in the smoke inhaled contain 0.1 to 2.8 milligrams of nicotine.14 Research15 suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use. A 21 mg patch applied to the left arm A 21 mg patch applied to the left arm Nicotine gum, usually in 2-mg or 4-mg doses, and nicotine patches are available, that do not have all the other ingredients in smoked tobacco. They appear to be not as addictive or as pleasurable, and, it is claimed, have fewer side effectscitation needed. Whether all the other psychoactive effects also occur has not been well studied. Dependence See also: Smoking cessation Modern research shows that nicotine acts on the brain to produce a number of effects. Specifically, its addictive nature has been found to show that nicotine activates reward pathways-the circuitry within the brain that regulates feelings of pleasure and euphoria.16 To reduce the health effects of cigarette smoking, the best thing to do is to quit. Public health authorities do not endorse either smoking fewer cigarettes or switching to lower tar and nicotine brands as a satisfactory way of reducing risk.17 Dopamine is one of the key neurotransmitters actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin, though chronic treatment has an opposite effect on reward thresholds. Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse namely cocaine and heroin, which reduce reward pathway sensitivitycitation needed. This neuronal brain alteration persists for months after administration ceases. Due to an increase in reward pathway sensitivity, nicotine withdrawal is relatively mild compared to ethanol or heroin withdrawal.citation needed Nicotine also has the potential to cause dependence in many animals other than humans. Mice have been administered nicotine and exhibit withdrawal reactions when its administration is stopped.18 A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescent.19 Toxicology The LD50 of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 40-60 mg 0.5-1.0 mg/kg can be a lethal dosage for adult humans.2021 This designates nicotine as an extremely deadly poison. It is more toxic than many other alkaloids such as cocaine, which has an LD50 of 95.1 mg/kg when administered to mice. Spilling a sufficient concentration of nicotine onto the skin can result in poisoning or even death since Nicotine readily passes into the bloodstream from dermal contact. 22 The carcinogenic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the IARC, and it has not been assigned to an official carcinogen group. The currently available literature indicates that nicotine, on its own, does not promote the development of cancer in healthy tissue and has no mutagenic properties. Its teratogenic properties have not yet been adequately researched, and while the likelihood of birth defects caused by nicotine is believed to be very small or nonexistent, nicotine replacement product manufacturers recommend consultation with a physician before using a nicotine patch or nicotine gum while pregnant or nursing. However, nicotine and the increased cholinergic activity it causes have been shown to impede apoptosiscitation needed, which is one of the methods by which the body destroys unwanted cells programmed cell death. Since apoptosis helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favourable environment for cancer to develop, though this also remains to be proven. Nicotine and oxidative stress Nicotine is detoxified by the cytochrome p450 in the liver. Recently it has been published that it produces free radicals in this reaction.citation needed Link to circulatory disease Nicotine has very powerful effects on arteries throughout the body. Nicotine is a stimulant, speeding up the heart by about 20 beats per minute with every cigarette; it raises blood pressure, and is a vasoconstrictor, making it harder for the heart to pump through the constricted arteries. It causes the body to release its stores of fat and cholesterol into the blood. Nicotine increases the risk of blood clots significantly.citation needed If blood clots in an artery, blood flow is reduced or halted, and tissue loses its source of oxygen and nutrients and dies in minutes. Peripheral circulation, arteries going to the extremities, are also highly susceptible to the vasoconstrictor effects of nicotine as well as the increased risk of clots and clogging.citation needed Therapeutic uses The primary therapeutic use of nicotine is in treating nicotine dependence in order to eliminate smoking with its risks to health. Controlled levels of nicotine are given to patients through gums, dermal patches, lozenges, electric/substitute cigarettes or nasal sprays in an effort to wean them off their dependence. However, in a few situations, smoking has been observed to apparently be of therapeutic value to patients. These are often referred to as Smoker's Paradoxes.23 Although in most cases the actual mechanism is understood only poorly or not at all, it is generally believed that the principal beneficial action is due to the nicotine administered, and that administration of nicotine without smoking may be as beneficial as smoking, without the higher risk to health due to tar and other ingredients found in tobacco. For instance, recent studies suggest that smokers require less frequent repeated revascularization after percutaneous coronary intervention PCI.23 Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking.2425 Smoking also appears to interfere with development of Kaposi's sarcoma,26 breast cancer among women carrying the very high risk BRCA gene,27 preeclampsia,28 and atopic disorders such as allergic asthma.29 A plausible mechanism of action in these cases may be nicotine acting as an anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.30 With regard to neurological diseases, a large body of evidence suggests that the risks of Parkinson's disease or Alzheimer's disease might be twice as high for non-smokers than for smokers.31 Many such papers regarding Alzheimer's disease32 and Parkinson's Disease33 have been published. More recent studies find that there's no beneficial link between smoking and Alzheimer's, and in some cases suggest that it actually results in an earlier onset of the disease.34 35 36 37 Recent studies have indicated that nicotine can be used to help adults suffering from Autosomal dominant nocturnal frontal lobe epilepsy. The same areas that cause seizures in that form of epilepsy are also responsible for processing nicotine in the brain.38 It has been noted that the majority of people diagnosed with schizophrenia smoke tobacco. Estimates for the number of schizophrenics that smoke range from 75% to 90%. It was recently argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine.39 40 More recent research has found the reverse, that it is a risk factor without long-term benefit, used only for its short term effects.41 However, research on nicotine as administered through a patch or gum is ongoing. Nicotine and its metabolites are being researched for the treatment of a number of disorders, including ADHD, Schizophrenia and Parkinson's Disease.42 People with schizophrenia smoke two to three times more than smokers without mental illness; this may be a form of self-medication to improve attention and short-term memory.43 The therapeutic use of nicotine as a means of appetite-control and to promote weight loss is anecdotally supported by many ex-smokers who claim to put on weight after quitting. Studies of nicotine in mice44 suggest it may play a role in weight-loss that is independent of appetite and studies involving the elderly suggest that nicotine affects not only weight loss, but also prevents some weight gain.45 See also Addiction Allen Carr Cigarette Dipping tobacco Drug addiction Myocardial infarction Nicogel Nicotini NicVAX Psychoactive drug Snuff Snus Stroke External links Description of nicotine addiction Description of nicotine mechanisms References ^ WHFoods: What are nightshades and in which foods are they found? ^ Smoking and Tobacco Control Monograph No. 9. ^ http://en..org/wiki/Ruyan#Ruyan_Electronic_Cigarette.2C_Ruyan_E-Cigarette_.28Ruyan_V8.29 ^ American Heart Association and Nicotine addiction. ^ Melsens 1844. Ueber das Nicotin. Journal für Praktische Chemie 32 1: 372-377. doi:10.1002/prac.18440320155. ^ Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. ^ Human Anatomy and Physiology. Elaine N Marieb Katja Hoehn. 2007, Pearson Education. ^ Paper published on PubMed ^ Fowler JS, Volkow ND, Wang GJ, Pappas N, Logan J, MacGregor R, Alexoff D, Wolf AP, Warner D, Cilento R, Zezulkova I 1998. Neuropharmacological actions of cigarette smoke: brain monoamine oxidase B MAO B inhibition. Journal of addictive diseases. PMID 9549600. ^ Gilbert Lagrue, François Lebargy, Anne Cormier, From nicotinic receptors to smoking dependence: therapeutic prospects Alcoologie et Addictologie Vol. : 23, N° : 2S, juin 2001, pages 39S - 42 ^ Jean-Claude Orsini, Dependence on tobacco smoking and brain systems controlling glycemia and appetite Alcoologie et Addictologie Vol. : 23, N° : 2S, juin 2001, pages 28S - 36S ^ Smokers lose their appetite : Media Releases : News : The University of Melbourne ^ Kenny PJ, Markou A. Nicotine self-administration acutely activates brain reward systems and induces a long-lasting increase in reward sensitivity Neuropsychopharmacology 2006 31, 1203-1211. ^ Erowid Nicotine Vault : Dosage ^ Einstein, Stanley 1989. Drug and Alcohol Use: Issues and Factors. Springer, 101-118. ISBN 0306413787. ^ NIDA - Research Report Series - Tobacco Addiction - Extent, Impact, Delivery, and Addictiveness ^ Smoking Health Issues - Philip Morris USA ^ NIDA - Publications - NIDA Notes - Vol. 19, No. 2 - Research Findings ^ Nolley E.P. Kelley B.M. Adolescent reward system perseveration due to nicotine: Studies with methylphenidate., Neurotoxicol Teratol., 2006 Oct 4 ^ Okamoto M., Kita T., Okuda H., Tanaka T., Nakashima T. 1994. Effects of aging on acute toxicity of nicotine in rats. Pharmacol Toxicol. 75 1: 1-6. ^ IPCS INCHEM ^ Lockhart LP 1933. Nicotine poisoning letter. Br Med J 1:246-247 ^ a b Cohen, David J.; Michel Doucet, Donald E. Cutlip, Kalon K.L. Ho, Jeffrey J. Popma, Richard E. Kuntz 2001. Impact of Smoking on Clinical and Angiographic Restenosis After Percutaneous Coronary Intervention. Circulation 104: 773. Retrieved on 2006-11-06. ^ Longmore, M., Wilkinson, I., Torok, E. Oxford Handbook of Clinical Medicine Fifth ion p. 232 ^ Green, JT; Richardson C, Marshall RW, Rhodes J, McKirdy HC, Thomas GA, Williams GT November, 2000. Nitric oxide mediates a therapeutic effect of nicotine in ulcerative colitis. Aliment Pharmacol Ther 14 11: 1429-1434. PMID : 11069313. Retrieved on 2006-11-06. ^ Smoking Cuts Risk of Rare Cancer in English, UPI March 29, 2001. Retrieved on 2006-11-06. ^ Recer, Paul May 19, 1998. Cigarettes May Have an Up Side in English, AP. Retrieved on 2006-11-06. ^ Lain, Kristine Y.; Robert W. Powers, Marijane A. Krohn, Roberta B. Ness, William R. Crombleholme, James M. Roberts November 1991. Urinary cotinine concentration confirms the reduced risk of preeclampsia with tobacco exposure. American Journal of Obstetrics and Gynecology 181 5: 908-14. PMID : 11422156. Retrieved on 2006-11-06. ^ Hjern, A; Hedberg A, Haglund B, Rosen M June 2001. Does tobacco smoke prevent atopic disorders? A study of two generations of Swedish residents. Clin Exp Allergy 31 6: 908-914. PMID : 11422156. Retrieved on 2006-11-06. ^ Lisa Melton June 2006. Body Blazes. Scientific American: p.24. ^ Fratiglioni, L; Wang HX August 2000. Smoking and Parkinson's and Alzheimer's disease: review of the epidemiological studies. Behav Brain Res 113 1-2: 117-120. PMID : 10942038. Retrieved on 2006-11-06. ^ Thompson, Carol. Alzheimer's disease is associated with non-smoking. Retrieved on 2006-11-06. ^ Thompson, Carol. Parkinson's disease is associated with non-smoking. Retrieved on 2006-11-06. ^ Alzheimer's Starts Earlier for Heavy Drinkers, Smokers. Reuters 2008-17-04. Retrieved on 2008-27-06. ^ Peck, Peggy 2002-25-07. Smoking Significantly Increases Risk of Alzheimer's Disease Among Those Who Have No Genetic Predisposition. Retrieved on 2008-27-06. ^ Aggarwal, Neelum, The Relation of Cigarette Smoking to Incident Alzheimer's Disease in a Biracial Urban Community Population, Neuroepidemiology 263: 140-146, doi:2006, http://content.karger.com/ProdukteDB/produkte.asp?Doi=91654. Retrieved on 2008-27-06 ^ Lerche Davis, Jeanie 2004-22-03. Smoking Speeds Dementia, Alzheimer's Disease. Retrieved on 2008-27-06. ^ Nicotine as an antiepileptic agent in ADNFLE: An n-of-one study. ^ Schizophr. Res. 2002 ^ Am. J. Psychiatry 1995 ^ Br. J. Psychiatry 2005 ^ Attention-Deficit Hyperactivity Disorder. Reuters Health. Reuters December 2001. Archived from the original on 2006-04-26. Nicotine improves ADHD symptoms. Although such findings should certainly not encourage anyone to smoke, some studies are focusing on benefits of nicotine therapy in adults with ADHD. ^ Nicotine Helps Schizophrenia Patients with Attention and Memory Problems ^ NIH, online at 1 ^ Cigarette Smoking and Weight Loss in Nursing Home Residents 2 Further reading Nicotine Therapy for ADNFLE: Nicotine as an antiepileptic agent in ADNFLE: An n-of-one study Minna, John D.: Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer Fallon, J.H., et al. 2005 Gender: A major determinant of brain response to nicotine. International Journal of Neuropharmacology. 8:1-10. 3 West, Kip A., et al.: Rapid Akt activation by nicotine and a tobacco carcinogen modulates the phenotype of normal human airway epithelial cells National Institute on Drug Abuse Erowid information on tobacco4 v d e Stimulants Alkylamines Cyclopentamine Geranamine Isometheptene Octodrine Propylhexedrine Tuamine Alphapyrrolidinylalkiophenones α-PPP MDPPP MDPV MPBP MPHP MPPP MOPPP Pyrovalerone Cholinergics ABT-089 ABT-418 Anabasine Arecoline Cotinine Cytisine Dianicline Epibatidine Epiboxidine GTS-21 Ispronicline Nicotine Rivanicline Tebanicline Varenicline Convulsants Bicuculline DMCM Gabazine Pentetrazol Picrotoxin Strychnine Thujone Eugeroics Adrafinil Armodafinil Carphedon Modafinil Phenethylamines 4-Bromomethcathinone 4-Fluoroamphetamine 4-Fluoromethamphetamine 4-Fluoromethcathinone 4-Methylmethcathinone 4-MTA Aletamine Amfepentorex Amphechloral Amphetamine Dextroamphetamine, Adderall Amphetaminil Benzphetamine Bupropion Cathinone Chlorphentermine Clenbuterol Clobenzorex Clortermine Diethylpropion Dimethoxyamphetamine Dimethylamphetamine Dimethylcathinone Ephedrine Epinephrine Ethcathinone Ethylamphetamine Fenethylline Fenfluramine Fenproporex Fludorex Furfenorex Levomethamphetamine Lisdexamfetamine MDMA Mefenorex Methamphetamine Methcathinone Methoxyphedrine Methylone Octopamine Ortetamine Parahydroxyamphetamine PCA PIA PMA PMEA PMMA PPAP Phendimetrazine Phenmetrazine Phentermine Phenylephrine Phenylpropanolamine Propylamphetamine Pseudoephedrine Selegiline Synephrine Tiflorex Xylopropamine Phenylaminooxazoles 4-Methyl-aminorex Aminorex Clominorex Fenozolone Fluminorex Pemoline Thozalinone Piperazines 2C-B-BZP BZP GBR-12783 GBR-12935 GBR-13069 GBR-13098 GBR-13119 MeOPP MBZP Vanoxerine Piperidines 2-Benzylpiperidine Desoxypipradrol Diphemethoxidine Ethylphenidate HDMP-28 --Methyl-1-methyl-4β-2-naphthylpiperidine-3β-carboxylate Methylphenidate Dexmethylphenidate Nocaine Phacetoperane Pipradrol Tropanes 3α-Bis-4-fluorophenylmethoxytropane 3α-4-Chlorophenylphenylmethoxytropane 3-Pseudotropyl-4-fluorobenzoate Altropane IACFT Brasofensine CFT WIN 35,428 β-CIT RTI-55 Cocaethylene Cocaine β-CPPIT Dichloropane RTI-111 Difluoropine FE-β-CPPIT FP-β-CPPIT PIT PTT RTI-31 RTI-32 RTI-51 RTI-112 RTI-113 RTI-121 IPCIT RTI-126 RTI-150 RTI-171 RTI-177 RTI-336 Tesofensine Troparil β-CPT, WIN 35,065-2 WF-23 WF-33 WF-60 Xanthines Aminophylline Caffeine Dimethazan Paraxanthine Theobromine Theophylline Others Amineptine Bemegride Benzydamine BPAP Bromantane BTQ Clofenciclan Cypenamine Cyprodenate Diclofensine Dimethocaine Diphenyl prolinol Ethamivan Fencamfamine Feprosidnine Gilutensin GYKI-52895 Hexacyclonate Indanorex Indatraline LR-5182 Mazindol Mesocarb Naphthylisopropylamine Nikethamide Nomifensine Phthalimidopropiophenone Prolintane Sibutramine Yohimbine Zylofuramine See also Sympathomimetic amines v d e Drugs used in addictive disorders N07B Nicotine dependence/ Nicotinic agonist Nicotine - Bupropion - Dianicline - Varenicline - Lobeline - Mecamylamine - Clonidine - Scopolamine - Surinabant Alcohol dependence Disulfiram - Calcium carbimide - Acamprosate - Naltrexone - Nalmefene - Topiramate - Clonidine - Buprenorphine - Morphine Opioid dependence Buprenorphine - Methadone - Levacetylmethadol - Fentanyl - Dihydrocodeine - Dihydroetorphine - Clonidine - Lofexidine - Naltrexone - Ibogaine - 18-Methoxycoronaridine - Extended Release Morphine - Extended Release Hydromorphone Stimulant dependence Dexamphetamine - Bupropion - Vanoxerine - Nocaine - Vigabatrin Benzodiazepine dependence Clonidine - Diazepam - Phenytoin - Phenobarbital Cocaine dependence Bupropion - Vanoxerine - Nocaine - Baclofen - Vigabatrin Sedative-Hypnotic dependence Phenobarbital - Diazepam - Lorazepam - Clonidine - Chloral Hydrate Retrieved from http://en..org/wiki/Nicotine Categories: Alkaloids | Health risks | Neurotoxins | Nitrogen heterocycles | Nicotinic agonists | Plant toxin insecticides | Pyridines | Pyrrolidines | Stimulants | Tobacco | SmokingHidden categories: All articles with statements | Articles with statements since April 2008 | Articles with statements since August 2008 | Articles with statements since July 2007 | Articles with statements since November 2007 | Articles with statements since April 2007 | Articles with statements since May 2008 | Articles with statements since February 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية БългарÑ?ки Català Česky Dansk Deutsch Eesti Ελληνικά Español Esperanto Ù?ارسی Français Galego í•œêµì–´ Bahasa Indonesia Ã?slenska Italiano עברית Kiswahili Lietuvių Magyar മലയാളം Bahasa Melayu Nederlands 日本語 ‪Norsk bokmÃ¥l‬ ‪Norsk nynorsk‬ Polski Português Română РуÑ?Ñ?кий Simple English SlovenÄ?ina SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Basa Sunda Suomi Svenska ไทย Tiếng Việt Türkçe ייִדיש ä¸æ–‡ This page was last modified on 19 August 2008, at 11:20
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