The adrenergic receptors (or adrenoceptors) are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine (noradrenaline) and epinephrine (adrenaline).
Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system. The sympathetic nervous system is responsible for the fight-or-flight response, which includes widening the pupils of the eye, mobilizing energy, and diverting blood flow from non-essential organs to skeletal muscle.
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Contents
- 1 Subtypes
- 1.1 Roles in circulation
- 1.2 Comparison
- 1.3 α receptors
- 1.3.1 α1 receptor
- 1.3.2 α2 receptor
- 1.4 β receptors
- 1.4.1 β1 receptor
- 1.4.2 β2 receptor
- 1.4.3 β3 receptor
- 2 See also
- 3 References
- 4 Further reading
- 5 External links
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Subtypes
History: Raymond Ahlquist, Professor of Pharmacology in Georgia, US, published a paper concerning adrenergic nervous transmission in 1948[1] but its significance was largely ignored at that time. However, in 1954 he was able to incorporate his findings in a textbook, Drill's Pharmacology in Medicine, and thereby firmly establish the essential role played by alpha and beta receptor sites in the adrenaline/nor-adrenaline cellular mechanism. His discovery would revolutionise advances in pharmacotherapeutic research, allowing the selective design of specific molecules to target medical ailments rather than rely upon traditional research into the efficacy of pre-existing herbal medicines.
There are two main groups of adrenergic receptors, α and β, with several subtypes.
- α receptors have the subtypes α1 (a Gq coupled receptor) and α2 (a Gi coupled receptor). Phenylephrine is a selective agonist of the α receptor.
- β receptors have the subtypes β1, β2 and β3. All three are linked to Gs proteins (although β2 also couples to Gi),[2] which in turn are linked to adenylate cyclase. Agonist binding thus causes a rise in the intracellular concentration of the second messenger cAMP. Downstream effectors of cAMP include cAMP-dependent protein kinase (PKA), which mediates some of the intracellular events following hormone binding. Isoprenaline is a non-selective agonist.
The mechanism of adrenergic receptors. Adrenaline or noradrenaline are receptor ligands to either α
1, α
2 or β-adrenergic receptors. α
1 couples to G
q, which results in increased intracellular Ca
2+ which results in smooth muscle contraction. α
2, on the other hand, couples to G
i, which causes a decrease of cAMP activity, resulting in smooth muscle contraction. β receptors couple to G
s, and increases intracellular cAMP activity, resulting in e.g. heart muscle contraction, smooth muscle relaxation and glycogenolysis.
Roles in circulation
Adrenaline (epinephrine) reacts with both α- and β-adrenoreceptors, causing vasoconstriction and vasodilation, respectively. Although α receptors are less sensitive to epinephrine, when activated, they override the vasodilation mediated by β-adrenoreceptors. The result is that high levels of circulating epinephrine cause vasoconstriction. At lower levels of circulating epinephrine, β-adrenoreceptor stimulation dominates, producing an overall vasodilation.
Comparison
Smooth muscle behavior is variable depending on anatomical location. Smooth muscle contraction/relaxation is generalized below. One important note is the differential effects of increased cAMP in smooth muscle compared to cardiac muscle. Increased cAMP will promote relaxation in smooth muscle, while promoting increased contractility and pulse rate in cardiac muscle.
| Receptor |
Agonist potency order |
Selected action
of agonist |
Mechanism |
Agonists |
Antagonists |
α1:
A, B, D† |
Norepinephrine > epinephrine >> isoprenaline |
Smooth muscle contraction |
Gq: phospholipase C (PLC) activated, IP3,and DAG, rise in calcium |
(Alpha-1 agonists)
- Noradrenaline
- Phenylephrine
- Methoxamine
- Cirazoline
- Xylometazoline
- Midodrine
- Metaraminol
|
(Alpha-1 blockers)
- Alfuzosin
- Doxazosin
- Phenoxybenzamine
- Phentolamine
- Prazosin
- Tamsulosin
- Terazosin
(TCA:s)
- Amitriptyline
- Clomipramine
- Doxepin
- Trimipramine
|
α2:
A, B, C |
Epinephrine ≥ norepinephrine >> isoprenaline |
Smooth muscle mixed effects and neurotransmitter inhibition & Cardiac muscle relaxation platelet activation |
Gi: adenylate cyclase inactivated, cAMP down |
(Alpha-2 agonists)
- Dexmedetomidine
- Medetomidine
- Romifidine
- Clonidine
- Brimonidine
- Detomidine
- Lofexidine
- Xylazine
- Tizanidine
- Guanfacine
- Amitraz
|
(Alpha-2 blockers)
- Phentolamine
- Yohimbine
- Idazoxan
- Atipamezole
|
| β1 |
Isoprenaline > epinephrine = norepinephrine |
Heart muscle contraction |
Gs: adenylate cyclase activated, cAMP up |
- Dobutamine
- Isoprenaline
- Noradrenaline
|
(Beta blockers)
- Metoprolol
- Atenolol
- Bisoprolol
|
| β2 |
Isoprenaline > epinephrine >> norepinephrine |
Smooth muscle relaxation |
Gs: adenylate cyclase activated, cAMP up (also Gi, see β2) |
(Short/long)
- Salbutamol (Albuterol in USA)
- Bitolterol mesylate
- Formoterol
- Isoprenaline
- Levalbuterol
- Metaproterenol
- Salmeterol
- Terbutaline
- Ritodrine
|
(Beta blockers)
|
| β3 |
Isoprenaline = norepinephrine > epinephrine |
Enhance lipolysis, promotes relaxation of detrusor muscle in the bladder |
Gs: adenylate cyclase activated, cAMP up |
- L-796568[3]
- Amibegron
- Solabegron
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†There is no α1C receptor. At one time, there was a subtype known as C, but was found to be identical to one of the previously discovered subtypes. To avoid confusion, naming was continued with the letter D.
α receptors
α receptors have several functions in common, but also individual effects. Common (or still unspecified) effects include:
- Vasoconstriction of arteries to heart (coronary artery).[4]
- Vasoconstriction of veins[5]
- Decrease motility of smooth muscle in gastrointestinal tract[6]
α1 receptor
Main article: Alpha-1 adrenergic receptor
Alpha1-adrenergic receptors are members of the G protein-coupled receptor superfamily. Upon activation, a heterotrimeric G protein, Gq, activates phospholipase C (PLC). The PLC cleaves phosphatidylinositol 4,5-bisphosphate (PIP2), which in turn causes an increase in inositol triphosphate (IP3) and diacylglycerol (DAG). The former interacts with calcium channels of endoplasmic and sarcoplasmic reticulum, thus changing the calcium content in a cell. This triggers all other effects.
Specific actions of the α1 receptor mainly involve smooth muscle contraction. It causes vasoconstriction in many blood vessels, including those of the skin, gastrointestinal system, kidney (renal artery)[7] and brain.[8] Other areas of smooth muscle contraction are:
- ureter
- vas deferens
- hair (arrector pili muscles)
- uterus (when pregnant)
- urethral sphincter
- bronchioles (although minor due to the relaxing effect of β2 receptor on bronchioles)
- blood vessels of ciliary body (stimulation causes mydriasis)
Further effects include glycogenolysis and gluconeogenesis from adipose tissue[9] and liver, as well as secretion from sweat glands[9] and Na+ reabsorption from kidney.[9]
Antagonists may be used in hypertension.
α2 receptor
Main article: Alpha-2 adrenergic receptor
There are 3 highly homologous subtypes of α2 receptors: α2A, α2Β, and α2C.
Specific actions of the α2 receptor include:
- inhibition of insulin release in the pancreas.[9]
- induction of glucagon release from the pancreas.
- contraction of sphincters of the gastrointestinal tract
- negative feedback in the neuronal synapses - presynaptic inhibition of noradrenalin release in CNS
- increased thrombocyte aggregation
β receptors
β1 receptor
Main article: Beta-1 adrenergic receptor
Specific actions of the β1 receptor include:
- Increase cardiac output by increasing heart rate (positive chronotropic effect), conduction velocity (positive dromotropic effect), and stroke volume (by enhancing contractility—positive inotropic effect).
- Increase renin secretion from juxtaglomerular cells of the kidney.
- Increase ghrelin secretion from the stomach.[10]
β2 receptor
Main article: Beta-2 adrenergic receptor
Specific actions of the β2 receptor include the following:
- Smooth muscle relaxation, e.g. in bronchi,[9] GI tract (decreased motility).
- Lipolysis in adipose tissue.[11]
- Anabolism in skeletal muscle.[12][13]
- Relax non-pregnant uterus
- Relax detrusor urinae muscle of bladder wall
- Dilate arteries to skeletal muscle
- Glycogenolysis and gluconeogenesis
- Stimulates insulin secretion
- Contract sphincters of GI tract
- Thickened secretions from salivary glands.[9]
- Inhibit histamine-release from mast cells
- Increase renin secretion from kidney
- Relaxation of Bronchioles (salbutamol, a beta 2 agonist relieves bronchiole constriction)
- Involved in brain - immune communication[14]
β3 receptor
Main article: Beta-3 adrenergic receptor
Specific actions of the β3 receptor include:
- Enhancement of lipolysis in adipose tissue. Beta-3 activating drugs could theoretically be used as weight-loss agents, but are limited by the side effect of tremors.
See also
- Beta adrenergic receptor kinase
- Beta adrenergic receptor kinase-2
References
- ^ Ahlquist R.P. A Study of the Adenotrophic Receptors, Am. J. Physiol. 1948 153:586-600
- ^ Chen-Izu Y, Xiao RP, Izu LT, Cheng H, Kuschel M, Spurgeon H, Lakatta EG (November 2000). "G(i)-dependent localization of beta(2)-adrenergic receptor signaling to L-type Ca(2+) channels". Biophys. J. 79 (5): 2547–56. doi:10.1016/S0006-3495(00)76495-2. PMC 1301137. PMID 11053129. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1301137/.
- ^ Nisoli E, Tonello C, Landi M, Carruba MO (1996). "Functional studies of the first selective β3-adrenergic receptor antagonist SR 59230A in rat brown adipocytes". Mol. Pharmacol. 49 (1): 7–14. PMID 8569714. http://molpharm.aspetjournals.org/cgi/content/abstract/49/1/7.
- ^ Woodman OL, Vatner SF (1987). "Coronary vasoconstriction mediated by α1- and α2-adrenoceptors in conscious dogs". Am. J. Physiol. 253 (2 Pt 2): H388–93. PMID 2887122. http://ajpheart.physiology.org/cgi/content/abstract/253/2/H388.
- ^ Elliott J (1997). "Alpha-adrenoceptors in equine digital veins: evidence for the presence of both α1- and α2-receptors mediating vasoconstriction". J. Vet. Pharmacol. Ther. 20 (4): 308–17. doi:10.1046/j.1365-2885.1997.00078.x. PMID 9280371.
- ^ Sagrada A, Fargeas MJ, Bueno L (1987). "Involvement of α1 and α2 adrenoceptors in the postlaparotomy intestinal motor disturbances in the rat". Gut 28 (8): 955–9. doi:10.1136/gut.28.8.955. PMC 1433140. PMID 2889649. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1433140/.
- ^ Schmitz JM, Graham RM, Sagalowsky A, Pettinger WA (1981). "Renal α1 and α2 adrenergic receptors: biochemical and pharmacological correlations". J. Pharmacol. Exp. Ther. 219 (2): 400–6. PMID 6270306. http://jpet.aspetjournals.org/cgi/content/abstract/219/2/400.
- ^ Circulation & Lung Physiology I M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
- ^ a b c d e f Fitzpatrick, David; Purves, Dale; Augustine, George (2004). "Table 20:2". Neuroscience (Third ed.). Sunderland, Mass: Sinauer. ISBN 0-87893-725-0.
- ^ Zhao, T. J.; Sakata, I.; Li, R. L.; Liang, G.; Richardson, J. A.; Brown, M. S. et al. (2010). "Ghrelin secretion stimulated by {beta}1-adrenergic receptors in cultured ghrelinoma cells and in fasted mice". Proc Natl Acad Sci U S A 107 (36): 15868–15873. doi:10.1073/pnas.1011116107. PMID 20713709.
- ^ Large V, Hellström L, Reynisdottir S, et al. (December 1997). "Human beta-2 adrenoceptor gene polymorphisms are highly frequent in obesity and associate with altered adipocyte beta-2 adrenoceptor function". J. Clin. Invest. 100 (12): 3005–13. doi:10.1172/JCI119854. PMC 508512. PMID 9399946. //www.ncbi.nlm.nih.gov/pmc/articles/PMC508512/.
- ^ Kline WO, Panaro FJ, Yang H, Bodine SC (February 2007). "Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol". J. Appl. Physiol. 102 (2): 740–7. doi:10.1152/japplphysiol.00873.2006. PMID 17068216.
- ^ Kamalakkannan G, Petrilli CM, George I, et al. (April 2008). "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure". J. Heart Lung Transplant. 27 (4): 457–61. doi:10.1016/j.healun.2008.01.013. PMID 18374884.
- ^ Elenkov, I. J., R. L. Wilder, et al. (2000). "The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system.". Pharmacol Rev 52 (4): 595–638. PMID 11121511.
Further reading
- Rang HP, Dale MM, Ritter JM, Moore PK (2003). "Chapter 11: Noradrenergic transmission". Pharmacology (5th ed.). Elsevier Churchill Livingstone. ISBN 0-443-07145-4.
- Rang HP, Dale MM, Ritter JM, Flower RJ (2007). "Chapter 11: Noradrenergic transmission". Rang and Dale's Pharmacology (6th ed.). Elsevier Churchill Livingstone. pp. 169–170. ISBN 0-443-06911-5.
External links
- Alpha receptors illustrated
- The Adrenergic Receptors
- "Adrenoceptors". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. http://www.iuphar-db.org/GPCR/ChapterMenuForward?chapterID=1274.
- Basic Neurochemistry: α- and β-Adrenergic Receptors
- Brief overview of functions of the beta-3 receptor
- Theory of receptor activation
- Desensitization of beta-1-receptors
- UMich Orientation of Proteins in Membranes protein/pdbid-2rh1 - 3D structure of beta-2 adrenergic receptor in membrane
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Adrenergics
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Receptor ligands
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α1
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- Agonists: 5-FNE
- 6-FNE
- Amidephrine
- Anisodamine
- Anisodine
- Cirazoline
- Dipivefrine
- Dopamine
- Ephedrine
- Epinephrine
- Etilefrine
- Ethylnorepinephrine
- Indanidine
- Levonordefrin
- Metaraminol
- Methoxamine
- Methyldopa
- Midodrine
- Naphazoline
- Norepinephrine
- Octopamine
- Oxymetazoline
- Phenylephrine
- Phenylpropanolamine
- Pseudoephedrine
- Synephrine
- Tetrahydrozoline
Antagonists: Abanoquil
- Adimolol
- Ajmalicine
- Alfuzosin
- Amosulalol
- Arotinolol
- Atiprosin
- Benoxathian
- Buflomedil
- Bunazosin
- Carvedilol
- CI-926
- Corynanthine
- Dapiprazole
- DL-017
- Domesticine
- Doxazosin
- Eugenodilol
- Fenspiride
- GYKI-12,743
- GYKI-16,084
- Indoramin
- Ketanserin
- L-765,314
- Labetalol
- Mephendioxan
- Metazosin
- Monatepil
- Moxisylyte
- Naftopidil
- Nantenine
- Neldazosin
- Nicergoline
- Niguldipine
- Pelanserin
- Phendioxan
- Phenoxybenzamine
- Phentolamine
- Piperoxan
- Prazosin
- Quinazosin
- Ritanserin
- RS-97,078
- SGB-1,534
- Silodosin
- SL-89.0591
- Spiperone
- Talipexole
- Tamsulosin
- Terazosin
- Tibalosin
- Tiodazosin
- Tipentosin
- Tolazoline
- Trimazosin
- Upidosin
- Urapidil
- Zolertine
- Note that many TCAs, TeCAs, antipsychotics, ergolines, and some piperazines like buspirone and trazodone all antagonize α1-adrenergic receptors as well, which contributes to their side effects such as orthostatic hypotension.
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α2
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- Agonists: (R)-3-Nitrobiphenyline
- 4-NEMD
- 6-FNE
- Amitraz
- Apraclonidine
- Brimonidine
- Cannabivarin
- Clonidine
- Detomidine
- Dexmedetomidine
- Dihydroergotamine
- Dipivefrine
- Dopamine
- Ephedrine
- Ergotamine
- Epinephrine
- Esproquin
- Etilefrine
- Ethylnorepinephrine
- Guanabenz
- Guanfacine
- Guanoxabenz
- Levonordefrin
- Lofexidine
- Medetomidine
- Methyldopa
- Mivazerol
- Naphazoline
- Norepinephrine
- Oxymetazoline
- Phenylpropanolamine
- Piperoxan
- Pseudoephedrine
- Rilmenidine
- Romifidine
- Talipexole
- Tetrahydrozoline
- Tizanidine
- Tolonidine
- Urapidil
- Xylazine
- Xylometazoline
Antagonists: 1-PP
- Adimolol
- Aptazapine
- Atipamezole
- BRL-44408
- Buflomedil
- Cirazoline
- Efaroxan
- Esmirtazapine
- Fenmetozole
- Fluparoxan
- GYKI-12,743
- GYKI-16,084
- Idazoxan
- Mianserin
- Mirtazapine
- MK-912
- NAN-190
- Olanzapine
- Phentolamine
- Phenoxybenzamine
- Piperoxan
- Piribedil
- Rauwolscine
- Rotigotine
- SB-269,970
- Setiptiline
- Spiroxatrine
- Sunepitron
- Tolazoline
- Yohimbine
* Note that many atypical antipsychotics and azapirones like buspirone (via metabolite 1-PP) antagonize α2-adrenergic receptors as well.
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β
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Reuptake inhibitors
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NET
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- Selective norepinephrine reuptake inhibitors: Amedalin
- Atomoxetine (Tomoxetine)
- Ciclazindol
- Daledalin
- Edivoxetine
- Esreboxetine
- Lortalamine
- Mazindol
- Nisoxetine
- Reboxetine
- Talopram
- Talsupram
- Tandamine
- Viloxazine; Norepinephrine-dopamine reuptake inhibitors: Amineptine
- Bupropion (Amfebutamone)
- Fencamine
- Fencamfamine
- Lefetamine
- Levophacetoperane
- LR-5182
- Manifaxine
- Methylphenidate
- Nomifensine
- O-2172
- Radafaxine; Serotonin-norepinephrine reuptake inhibitors: Bicifadine
- Desvenlafaxine
- Duloxetine
- Eclanamine
- Levomilnacipran
- Milnacipran
- Sibutramine
- Venlafaxine; Serotonin-norepinephrine-dopamine reuptake inhibitors: Brasofensine
- Diclofensine
- DOV-102,677
- DOV-21,947
- DOV-216,303
- JNJ-7925476
- JZ-IV-10
- Methylnaphthidate
- Naphyrone
- NS-2359
- PRC200-SS
- SEP-225,289
- SEP-227,162
- Tesofensine; Tricyclic antidepressants: Amitriptyline
- Butriptyline
- Cianopramine
- Clomipramine
- Desipramine
- Dosulepin
- Doxepin
- Imipramine
- Lofepramine
- melitracen
- Nortriptyline
- Protriptyline
- Trimipramine; Tetracyclic antidepressants: Amoxapine
- Maprotiline
- Mianserin
- Oxaprotiline
- Setiptiline; Others: Cocaine
- CP-39,332
- EXP-561
- Fezolamine
- Ginkgo biloba
- Indeloxazine
- Nefazodone
- Nefopam
- Pridefrine
- Tapentadol
- Tedatioxetine
- Teniloxazine
- Tofenacin
- Tramadol
- Ziprasidone
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VMAT
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- Ibogaine
- Reserpine
- Tetrabenazine
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Enzyme inhibitors
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Anabolism
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PAH
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TH
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- 3-Iodotyrosine
- Aquayamycin
- Bulbocapnine
- Metirosine
- Oudenone
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AAAD
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- Benserazide
- Carbidopa
- DFMD
- Genistein
- Methyldopa
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DBH
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- Bupicomide
- Disulfiram
- Dopastin
- Fusaric acid
- Nepicastat
- Phenopicolinic acid
- Tropolone
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PNMT
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- CGS-19281A
- SKF-64139
- SKF-7698
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Catabolism
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MAO
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- Nonselective: Benmoxin
- Caroxazone
- Echinopsidine
- Furazolidone
- Hydralazine
- Indantadol
- Iproclozide
- Iproniazid
- Isocarboxazid
- Isoniazid
- Linezolid
- Mebanazine
- Metfendrazine
- Nialamide
- Octamoxin
- Paraxazone
- Phenelzine
- Pheniprazine
- Phenoxypropazine
- Pivalylbenzhydrazine
- Procarbazine
- Safrazine
- Tranylcypromine; MAO-A selective: Amiflamine
- Bazinaprine
- Befloxatone
- Befol
- Brofaromine
- Cimoxatone
- Clorgiline
- Esuprone
- Harmala alkaloids (Harmine,
- Harmaline
- Tetrahydroharmine
- Harman
- Norharman, etc)
- Methylene blue
- Metralindole
- Minaprine
- Moclobemide
- Pirlindole
- Sercloremine
- Tetrindole
- Toloxatone
- Tyrima; MAO-B selective:
- Ladostigil
- Lazabemide
- Milacemide
- Mofegiline
- Pargyline
- Rasagiline
- Safinamide
- Selegiline (also [[D-Deprenyl]])
* Note that MAO-B inhibitors also influence norepinephrine/epinephrine levels since they inhibit the breakdown of their precursor dopamine.
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COMT
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- Entacapone
- Nitecapone
- Tolcapone
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Others
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Precursors
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- L-Phenylalanine → L-Tyrosine → L-DOPA (Levodopa) → Dopamine
- L-DOPS (Droxidopa)
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Cofactors
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- Ferrous Iron (Fe2+)
- S-Adenosyl-L-Methionine
- Vitamin B3 (Niacin
- Nicotinamide → NADPH)
- Vitamin B6 (Pyridoxine
- Pyridoxamine
- Pyridoxal → Pyridoxal Phosphate)
- Vitamin B9 (Folic acid → Tetrahydrofolic acid)
- Vitamin C (Ascorbic acid)
- Zinc (Zn2+)
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Others
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- Activity enhancers: BPAP
- PPAP; Release blockers: Bethanidine
- Bretylium
- Guanadrel
- Guanazodine
- Guanclofine
- Guanethidine
- Guanoxan; Toxins: 6-OHDA
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List of adrenergic drugs
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Cell surface receptor: G protein-coupled receptors
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Class A:
Rhodopsin like |
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| Class B: Secretin like |
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Orphan
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- GPR (56
- 64
- 97
- 98
- 110
- 111
- 112
- 113
- 114
- 115
- 116
- 123
- 124
- 125
- 126
- 128
- 133
- 143
- 144
- 155
- 157)
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Other
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- Brain-specific angiogenesis inhibitor (1
- 2
- 3)
- Cadherin (1
- 2
- 3)
- Calcitonin
- CALCRL
- CD97
- Corticotropin-releasing hormone (1
- 2)
- EMR (1
- 2
- 3)
- Glucagon (GR
- GIPR
- GLP1R
- GLP2R)
- Growth hormone releasing hormone
- PACAPR1
- GPR
- Latrophilin (1
- 2
- 3
- ELTD1)
- Methuselah-like proteins
- Parathyroid hormone (1
- 2)
- Secretin
- Vasoactive intestinal peptide (1
- 2)
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Class C: Metabotropic
glutamate / pheromone |
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Taste
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- TAS1R (1
- 2
- 3)
- TAS2R (1
- 3
- 4
- 5
- 7
- 8
- 9
- 10
- 13
- 14
- 16
- 19
- 20
- 30
- 31
- 38
- 39
- 40
- 41
- 42
- 43
- 45
- 46
- 50
- 60)
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Other
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- Calcium-sensing receptor
- GABA B (1
- 2)
- Glutamate receptor (Metabotropic glutamate (1
- 2
- 3
- 4
- 5
- 6
- 7
- 8))
- GPRC6A
- GPR (156
- 158
- 179)
- RAIG (1
- 2
- 3
- 4)
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Class F:
Frizzled / Smoothened |
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Frizzled
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- Frizzled (1
- 2
- 3
- 4
- 5
- 6
- 7
- 8
- 9
- 10)
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Smoothened
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B trdu: iter (nrpl/grfl/cytl/horl), csrc (lgic, enzr, gprc, igsr, intg, nrpr/grfr/cytr), itra (adap, gbpr, mapk), calc, lipd; path (hedp, wntp, tgfp+mapp, notp, jakp, fsap, hipp, tlrp)
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