ReceptorAgonist potency orderSelected actionofagonistMechanismAgonistsAntagonists

1:A,B,DNorepinephrine>epinephrine>>isoprenalineSmooth musclecontraction,mydriasis,vasoconstrictionin the skin, muscosa and abdominalviscera& sphincter contraction of theGI tractandurinary bladderGq:phospholipase C(PLC) activated,IP3,and DAG, rise incalcium(Alpha-1 agonists) Noradrenaline Phenylephrine Methoxamine Cirazoline Xylometazoline Midodrine Metaraminol Chloroethylclonidine(Alpha-1 blockers) Alfuzosin Doxazosin Phenoxybenzamine Phentolamine Prazosin Tamsulosin Terazosin Trazodone(TCA:s) Amitriptyline Clomipramine Doxepin Trimipramine Typical and atypical antipsychoticsAntihistamines(H1 antagonists) Hydroxyzine

2:A,B,CEpinephrinenorepinephrine>>IsoprenalineSmooth musclemixed effects, norepinephrine (noradrenaline) inhibition,plateletactivationGi:adenylate cyclaseinactivated,cAMPdown(Alpha-2 agonists) Agmatine Dexmedetomidine Medetomidine Romifidine Clonidine Chloroethylclonidine Brimonidine Detomidine Lofexidine Xylazine Tizanidine Guanfacine Amitraz(Alpha-2 blockers) Phentolamine Yohimbine Idazoxan Atipamezole Trazodone Typical and atypical antipsychotics

1Isoprenaline>epinephrine=norepinephrinePositiveChronotropic,Dromotropicandinotropiceffects, increasedamylasesecretionGs:adenylate cyclaseactivated,cAMPup Dobutamine Isoprenaline Noradrenaline(Beta blockers) Metoprolol Atenolol Bisoprolol Propranolol Timolol Nebivolol Vortioxetine

2Isoprenaline>epinephrine>>norepinephrineMuscle relaxation (Ex.Bronchodilation)Gs:adenylate cyclaseactivated,cAMPup (alsoGi, see2)(Short/long) Salbutamol(Albuterol in USA) Bitolterol mesylate Formoterol Isoprenaline Levalbuterol Metaproterenol Salmeterol Terbutaline Ritodrine(Beta blockers) Butoxamine Timolol Propranolol

3Isoprenaline=norepinephrine>epinephrineEnhance lipolysis, promotes relaxation of detrusor in thebladderGs:adenylate cyclaseactivated,cAMPup L-796568[4] Amibegron Solabegron SR 59230A

[5]There is no 1Creceptor. 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. receptors receptors have several functions in common, but also individual effects. Common (or still unspecified) effects include: Vasoconstriction ofveins[6] Decrease motility ofsmooth muscleingastrointestinal tract[7]1receptor[edit]Main article:Alpha-1 adrenergic receptor1-adrenergic receptors are members of the Gqprotein-coupled receptor superfamily. Upon activation, a heterotrimeric G protein, Gq, activates phospholipase C (PLC). The PLC cleavesphosphatidylinositol 4,5-bisphosphate(PIP2), which in turn causes an increase ininositol triphosphate(IP3) anddiacylglycerols(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 1receptor mainly involve smooth muscle contraction. It causesvasoconstrictionin manyblood vessels, including those of theskin,gastrointestinal system,kidney(renal artery)[8]andbrain.[9]Other areas of smooth muscle contraction are: ureter vas deferens hair(arrector pili muscles) uterus(when pregnant) urethral sphincter urotheliumandlamina propria[10] bronchioles(although minor due to the relaxing effect of 2receptor on bronchioles) blood vessels of ciliary body (stimulation causesmydriasis)Further effects includeglycogenolysisandgluconeogenesisfromadipose tissue[11]andliver, as well as secretion fromsweat glands[11]andNa+reabsorption fromkidney.[11]Antagonists may be used primarily inhypertension,anxiety disorder, andpanic attacks.2receptorsMain article:Alpha-2 adrenergic receptorThe 2receptor couples to the Gi/oprotein.[2]It is a presynaptic receptor, causing negative feedback on, for example, norepinephrine. When NA is released into the synapse, it feeds back on the 2receptor, causing less NA release from the presynaptic neuron. This decreases the effect of NA. There are also 2receptors on the nerve terminal membrane of the post-synaptic adrenergic neuron.There are 3 highly homologous subtypes of 2receptors:2A,2, and2C.Specific actions of the 2receptor include: Inhibition ofinsulinrelease in thepancreas.[11] Induction ofglucagonrelease from the pancreas. contraction ofsphinctersof thegastrointestinal tract negative feedback in the neuronal synapses - presynaptic inhibition of noradrenalin (NA) release in CNS increased thrombocyte aggregation receptors[edit]1receptor[edit]Main article:Beta-1 adrenergic receptorSpecific actions of the 1receptor include: Increasecardiac outputby increasing heart rate (positive chronotropic effect), conduction velocity (positive dromotropic effect), and stroke volume (by enhancing contractilitypositive inotropic effect). Increasereninsecretion fromjuxtaglomerular cellsof the kidney. Increaseghrelinsecretion from the stomach.[12]2receptor[edit]Main article:Beta-2 adrenergic receptor

Beta-2 adrenergic receptor (PDB2rh1), which stimulates cells to increase energy production and utilization. The membrane is shown schematically with a gray stripe.Specific actions of the 2receptor include the following: Smooth musclerelaxation, e.g. inbronchi,[11]GI tract(decreased motility). Lipolysisinadipose tissue.[13] Anabolisminskeletal muscle.[14][15] Relax non-pregnantuterus Relaxdetrusor urinae muscleofbladderwall Dilatearteriestoskeletal muscle Glycogenolysisandgluconeogenesis Inhibitsinsulinsecretion ContractsphinctersofGI tract Thickened secretions fromsalivary glands.[11] Inhibithistamine-release frommast cells Increasereninsecretion fromkidney Relaxation of Bronchioles (salbutamol, a 2agonist relieves bronchiole constriction) Involved in brain - immune communication[16]3receptor[edit]Main article:Beta-3 adrenergic receptorSpecific actions of the 3receptor include: Enhancement oflipolysisinadipose tissue. 3activating drugs could theoretically be used as weight-loss agents, but are limited by the side effect of tremors.