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The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines like norepinephrine (noradrenaline) and epinephrine (adrenaline) produced by the body, but also many medications like beta blockers, beta-2 (β2) agonists and alpha-2 (α2) agonists, which are used to treat high blood pressure and asthma, for example.

β2 adrenoceptor (PDB: 2rh1​) shown binding carazolol (yellow) on its extracellular site. β2 stimulates cells to increase energy production and utilization. The membrane the receptor is bound to in cells is shown with a gray stripe.

Many cells have these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system (SNS). The SNS is responsible for the fight-or-flight response, which is triggered by experiences such as exercise or fear-causing situations. This response dilates pupils, increases heart rate, mobilizes energy, and diverts blood flow from non-essential organs to skeletal muscle. These effects together tend to increase physical performance momentarily.

Contents

By the turn of the 19th century, it was agreed that the stimulation of sympathetic nerves could cause different effects on body tissues, depending on the conditions of stimulation (such as the presence or absence of some toxin). Over the first half of the 20th century, two main proposals were made to explain this phenomenon:

  1. There were (at least) two different types of neurotransmitters released from sympathetic nerve terminals, or
  2. There were (at least) two different types of detector mechanisms for a single neurotransmitter.

The first hypothesis was championed by Walter Bradford Cannon and Arturo Rosenblueth, who interpreted many experiments to then propose that there were two neurotransmitter substances, which they called sympathin E (for 'excitation') and sympathin I (for 'inhibition').

The second hypothesis found support from 1906 to 1913, when Henry Hallett Dale explored the effects of adrenaline (which he called adrenine at the time), injected into animals, on blood pressure. Usually, adrenaline would increase the blood pressure of these animals. Although, if the animal had been exposed to ergotoxine, the blood pressure decreased. He proposed that the ergotoxine caused "selective paralysis of motor myoneural junctions" (i.e. those tending to increase the blood pressure) hence revealing that under normal conditions that there was a "mixed response", including a mechanism that would relax smooth muscle and cause a fall in blood pressure. This "mixed response", with the same compound causing either contraction or relaxation, was conceived of as the response of different types of junctions to the same compound.

This line of experiments were developed by several groups, including DT Marsh and colleagues, who in February 1948 showed that a series of compounds structurally related to adrenaline could also show either contracting or relaxing effects, depending on whether or not other toxins were present. This again supported the argument that the muscles had two different mechanisms by which they could respond to the same compound. In June of that year, Raymond Ahlquist, Professor of Pharmacology at Medical College of Georgia, published a paper concerning adrenergic nervous transmission. In it, he explicitly named the different responses as due to what he called α receptors and β receptors, and that the only sympathetic transmitter was adrenaline. While the latter conclusion was subsequently shown to be incorrect (it is now known to be noradrenaline), his receptor nomenclature and concept of two different types of detector mechanisms for a single neurotransmitter, remains. In 1954, he was able to incorporate his findings in a textbook, Drill's Pharmacology in Medicine, and thereby promulgate the role played by α and β receptor sites in the adrenaline/noradrenaline cellular mechanism. These concepts 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.

The mechanism of adrenoreceptors. Adrenaline or noradrenaline are receptor ligands to either α1, α2 or β-adrenoreceptors. α1 couples to Gq, which results in increased intracellular Ca2+ and subsequent smooth muscle contraction. α2, on the other hand, couples to Gi, which causes a decrease in neurotransmitter release, as well as a decrease of cAMP activity resulting in smooth muscle contraction. β receptors couple to Gs, and increases intracellular cAMP activity, resulting in e.g. heart muscle contraction, smooth muscle relaxation and glycogenolysis.

There are two main groups of adrenoreceptors, α and β, with 9 subtypes in total:

  • α are divided to α1 (a Gq coupled receptor) and α2 (a Gi coupled receptor)
    • α1 has 3 subtypes: α1A, α1B and α1D
    • α2 has 3 subtypes: α2A, α2B and α2C
  • β are divided to β1, β2 and β3. All 3 are coupled to Gs proteins, but β2 and β3 also couple to Gi

Gi and Gs are linked to adenylyl cyclase. Agonist binding thus causes a rise in the intracellular concentration of the second messenger (Gi inhibits the production of cAMP) cAMP. Downstream effectors of cAMP include cAMP-dependent protein kinase (PKA), which mediates some of the intracellular events following hormone binding.

Roles in circulation

Epinephrine (adrenaline) reacts with both α- and β-adrenoreceptors, causing vasoconstriction and vasodilation, respectively. Although α receptors are less sensitive to epinephrine, when activated at pharmacologic doses, they override the vasodilation mediated by β-adrenoreceptors because there are more peripheral α1 receptors than β-adrenoreceptors. The result is that high levels of circulating epinephrine cause vasoconstriction. However, the opposite is true in the coronary arteries, where β2 response is greater than that of α1, resulting in overall dilation with increased sympathetic stimulation. At lower levels of circulating epinephrine (physiologic epinephrine secretion), β-adrenoreceptor stimulation dominates since epinephrine has a higher affinity for the β2 adrenoreceptor than the α1 adrenoreceptor, producing vasodilation followed by decrease of peripheral vascular resistance.

Subtypes

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 Agonist action Mechanism Agonists Antagonists
α1: A, B, D Norepinephrine > epinephrine >> isoprenaline Smooth muscle contraction, mydriasis, vasoconstriction in the skin, mucosa and abdominal viscera & sphincter contraction of the GI tract and urinary bladder Gq: phospholipase C (PLC) activated, IP3, and DAG, rise in calcium

(Alpha-1 agonists)

(Alpha-1 blockers)

(TCAs)

Antihistamines (H1 antagonists)

α2: A, B, C Epinephrine = norepinephrine >> isoprenaline Smooth muscle mixed effects, norepinephrine (noradrenaline) inhibition, platelet activation Gi: adenylate cyclase inactivated, cAMP down

(Alpha-2 agonists)

(Alpha-2 blockers)
β1 Isoprenaline > norepinephrine > epinephrine Positive chronotropic, dromotropic and inotropic effects, increased amylase secretion Gs: adenylate cyclase activated, cAMP up (β1-adrenergic agonist) (Beta blockers)
β2 Isoprenaline > epinephrine > norepinephrine Smooth muscle relaxation (bronchodilation for example) Gs: adenylate cyclase activated, cAMP up (also Gi, see α2) (β2-adrenergic agonist) (Beta blockers)
β3 Isoprenaline > norepinephrine = epinephrine Enhance lipolysis, promotes relaxation of detrusor muscle in the bladder Gs: adenylate cyclase activated, cAMP up (also Gi, see α2) (β3-adrenergic agonist) (Beta blockers)

α receptors

α receptors have actions in common, but also individual effects. Common (or still receptor unspecified) actions include:

Subtype unspecific α agonists (see actions above) can be used to treat rhinitis (they decrease mucus secretion). Subtype unspecific α antagonists can be used to treat pheochromocytoma (they decrease vasoconstriction caused by norepinephrine).

α1 receptor

α1-adrenoreceptors are members of the Gq 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, including a prominent slow after depolarizing current (sADP) in neurons.

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) and brain. Other areas of smooth muscle contraction are:

Actions also include glycogenolysis and gluconeogenesis from adipose tissue and liver; secretion from sweat glands and Na+ reabsorption from kidney.

α1 antagonists can be used to treat:

α2 receptor

The α2 receptor couples to the Gi/o protein. It is a presynaptic receptor, causing negative feedback on, for example, norepinephrine (NE). When NE is released into the synapse, it feeds back on the α2 receptor, causing less NE release from the presynaptic neuron. This decreases the effect of NE. There are also α2 receptors on the nerve terminal membrane of the post-synaptic adrenergic neuron.

Actions of the α2 receptor include:

α2 agonists (see actions above) can be used to treat:

α2 antagonists can be used to treat:

β receptors

Subtype unspecific β agonists can be used to treat:

Subtype unspecific β antagonists (beta blockers) can be used to treat:

β1 receptor

Actions of the β1 receptor include:

  • increase cardiac output by increasing heart rate (positive chronotropic effect), conduction velocity (positive dromotropic effect), stroke volume (by enhancing contractility – positive inotropic effect), and rate of relaxation of the myocardium, by increasing calcium ion sequestration rate (positive lusitropic effect), which aids in increasing heart rate
  • increase renin secretion from juxtaglomerular cells of the kidney
  • increase renin secretion from kidney
  • increase ghrelin secretion from the stomach

β2 receptor

Actions of the β2 receptor include:

β2 agonists (see actions above) can be used to treat:

β3 receptor

Actions of the β3 receptor include:

β3 agonists could theoretically be used as weight-loss drugs, but are limited by the side effect of tremors.

  1. There is no α1C receptor. There was a subtype known as C, but it was found to be identical to one of the previously discovered subtypes. To avoid confusion, naming was continued with the letter D. Before June 1995 α1A was named α1C. α1D was named α1A, α1D or α1A/D.
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Adrenergic receptor Article Talk Language Watch Edit 160 160 Redirected from B adrenergic The adrenergic receptors or adrenoceptors are a class of G protein coupled receptors that are targets of many catecholamines like norepinephrine noradrenaline and epinephrine adrenaline produced by the body but also many medications like beta blockers beta 2 b2 agonists and alpha 2 a2 agonists which are used to treat high blood pressure and asthma for example b2 adrenoceptor PDB 2rh1 shown binding carazolol yellow on its extracellular site b2 stimulates cells to increase energy production and utilization The membrane the receptor is bound to in cells is shown with a gray stripe Many cells have these receptors and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system SNS The SNS is responsible for the fight or flight response which is triggered by experiences such as exercise or fear causing situations This response dilates pupils increases heart rate mobilizes energy and diverts blood flow from non essential organs to skeletal muscle These effects together tend to increase physical performance momentarily Contents 1 History 2 Categories 2 1 Roles in circulation 2 2 Subtypes 2 3 a receptors 2 3 1 a1 receptor 2 3 2 a2 receptor 2 4 b receptors 2 4 1 b1 receptor 2 4 2 b2 receptor 2 4 3 b3 receptor 3 See also 4 Notes 5 References 6 Further reading 7 External linksHistory EditMain article History of catecholamine research Epinephrine Norepinephrine By the turn of the 19th century it was agreed that the stimulation of sympathetic nerves could cause different effects on body tissues depending on the conditions of stimulation such as the presence or absence of some toxin Over the first half of the 20th century two main proposals were made to explain this phenomenon There were at least two different types of neurotransmitters released from sympathetic nerve terminals or There were at least two different types of detector mechanisms for a single neurotransmitter The first hypothesis was championed by Walter Bradford Cannon and Arturo Rosenblueth 1 who interpreted many experiments to then propose that there were two neurotransmitter substances which they called sympathin E for excitation and sympathin I for inhibition The second hypothesis found support from 1906 to 1913 when Henry Hallett Dale explored the effects of adrenaline which he called adrenine at the time injected into animals on blood pressure Usually adrenaline would increase the blood pressure of these animals Although if the animal had been exposed to ergotoxine the blood pressure decreased 2 3 He proposed that the ergotoxine caused selective paralysis of motor myoneural junctions i e those tending to increase the blood pressure hence revealing that under normal conditions that there was a mixed response including a mechanism that would relax smooth muscle and cause a fall in blood pressure This mixed response with the same compound causing either contraction or relaxation was conceived of as the response of different types of junctions to the same compound This line of experiments were developed by several groups including DT Marsh and colleagues 4 who in February 1948 showed that a series of compounds structurally related to adrenaline could also show either contracting or relaxing effects depending on whether or not other toxins were present This again supported the argument that the muscles had two different mechanisms by which they could respond to the same compound In June of that year Raymond Ahlquist Professor of Pharmacology at Medical College of Georgia published a paper concerning adrenergic nervous transmission 5 In it he explicitly named the different responses as due to what he called a receptors and b receptors and that the only sympathetic transmitter was adrenaline While the latter conclusion was subsequently shown to be incorrect it is now known to be noradrenaline his receptor nomenclature and concept of two different types of detector mechanisms for a single neurotransmitter remains In 1954 he was able to incorporate his findings in a textbook Drill s Pharmacology in Medicine 6 and thereby promulgate the role played by a and b receptor sites in the adrenaline noradrenaline cellular mechanism These concepts 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 Categories Edit The mechanism of adrenoreceptors Adrenaline or noradrenaline are receptor ligands to either a1 a2 or b adrenoreceptors a1 couples to Gq which results in increased intracellular Ca2 and subsequent smooth muscle contraction a2 on the other hand couples to Gi which causes a decrease in neurotransmitter release as well as a decrease of cAMP activity resulting in smooth muscle contraction b receptors couple to Gs and increases intracellular cAMP activity resulting in e g heart muscle contraction smooth muscle relaxation and glycogenolysis There are two main groups of adrenoreceptors a and b with 9 subtypes in total a are divided to a1 a Gq coupled receptor and a2 a Gi coupled receptor 7 a1 has 3 subtypes a1A a1B and a1D a a2 has 3 subtypes a2A a2B and a2C b are divided to b1 b2 and b3 All 3 are coupled to Gs proteins but b2 and b3 also couple to Gi 7 Gi and Gs are linked to adenylyl cyclase Agonist binding thus causes a rise in the intracellular concentration of the second messenger Gi inhibits the production of cAMP cAMP Downstream effectors of cAMP include cAMP dependent protein kinase PKA which mediates some of the intracellular events following hormone binding Roles in circulation Edit Epinephrine adrenaline reacts with both a and b adrenoreceptors causing vasoconstriction and vasodilation respectively Although a receptors are less sensitive to epinephrine when activated at pharmacologic doses they override the vasodilation mediated by b adrenoreceptors because there are more peripheral a1 receptors than b adrenoreceptors The result is that high levels of circulating epinephrine cause vasoconstriction However the opposite is true in the coronary arteries where b2 response is greater than that of a1 resulting in overall dilation with increased sympathetic stimulation At lower levels of circulating epinephrine physiologic epinephrine secretion b adrenoreceptor stimulation dominates since epinephrine has a higher affinity for the b2 adrenoreceptor than the a1 adrenoreceptor producing vasodilation followed by decrease of peripheral vascular resistance 8 Subtypes Edit 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 Agonist action Mechanism Agonists Antagonistsa1 A B D a Norepinephrine gt epinephrine gt gt isoprenaline 9 Smooth muscle contraction mydriasis vasoconstriction in the skin mucosa and abdominal viscera amp sphincter contraction of the GI tract and urinary bladder Gq phospholipase C PLC activated IP3 and DAG rise in calcium 7 Alpha 1 agonists Noradrenaline Phenylephrine Methoxamine Cirazoline Xylometazoline Midodrine Metaraminol Chloroethylclonidine Adrenoswitches photoswitchable agonists 10 Alpha 1 blockers Acepromazine Alfuzosin Doxazosin Phenoxybenzamine Phentolamine Prazosin Tamsulosin Terazosin Trazodone TCAs Clomipramine Doxepin Trimipramine Typical and atypical antipsychotics Antihistamines H1 antagonists Hydroxyzinea2 A B C Epinephrine norepinephrine gt gt isoprenaline 9 Smooth muscle mixed effects norepinephrine noradrenaline inhibition platelet activation Gi adenylate cyclase inactivated cAMP down 7 Alpha 2 agonists Agmatine Dexmedetomidine Medetomidine Romifidine Clonidine Chloroethylclonidine Brimonidine Detomidine Lofexidine Xylazine Tizanidine Guanfacine Amitraz Alpha 2 blockers Phenoxybenzamine Phentolamine Yohimbine Idazoxan Atipamezole Trazodone Typical and atypical antipsychoticsb1 Isoprenaline gt norepinephrine gt epinephrine 9 Positive chronotropic dromotropic and inotropic effects increased amylase secretion Gs adenylate cyclase activated cAMP up 7 b1 adrenergic agonist Dobutamine Isoprenaline Noradrenaline Beta blockers Metoprolol Atenolol Bisoprolol Propranolol Timolol Nebivolol Vortioxetineb2 Isoprenaline gt epinephrine gt norepinephrine 9 Smooth muscle relaxation bronchodilation for example Gs adenylate cyclase activated cAMP up also Gi see a2 7 b2 adrenergic agonist Salbutamol Albuterol in USA Bitolterol mesylate Formoterol Isoprenaline Levalbuterol Metaproterenol Salmeterol Terbutaline Ritodrine Beta blockers Butoxamine Timolol Propranolol ICI 118 551 Paroxetine 11 b3 Isoprenaline gt norepinephrine epinephrine 9 Enhance lipolysis promotes relaxation of detrusor muscle in the bladder Gs adenylate cyclase activated cAMP up also Gi see a2 7 b3 adrenergic agonist L 796568 12 Amibegron Solabegron Mirabegron Beta blockers SR 59230A a receptors Edit a receptors have actions in common but also individual effects Common or still receptor unspecified actions include vasoconstriction 13 decreased flow of smooth muscle in gastrointestinal tract 14 Subtype unspecific a agonists see actions above can be used to treat rhinitis they decrease mucus secretion Subtype unspecific a antagonists can be used to treat pheochromocytoma they decrease vasoconstriction caused by norepinephrine 7 a1 receptor Edit Main article Alpha 1 adrenergic receptor a1 adrenoreceptors are members of the Gq 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 including a prominent slow after depolarizing current sADP in neurons 15 Actions of the a1 receptor mainly involve smooth muscle contraction It causes vasoconstriction in many blood vessels including those of the skin gastrointestinal system kidney renal artery 16 and brain 17 Other areas of smooth muscle contraction are ureter vas deferens hair arrector pili muscles uterus when pregnant urethral sphincter urothelium and lamina propria 18 bronchioles although minor relative to the relaxing effect of b2 receptor on bronchioles blood vessels of ciliary body stimulation causes mydriasis Actions also include glycogenolysis and gluconeogenesis from adipose tissue and liver secretion from sweat glands and Na reabsorption from kidney 19 a1 antagonists can be used to treat 7 hypertension decrease blood pressure by decreasing peripheral vasoconstriction benign prostate hyperplasia relax smooth muscles within the prostate thus easing urinationa2 receptor Edit Main article Alpha 2 adrenergic receptor The a2 receptor couples to the Gi o protein 20 It is a presynaptic receptor causing negative feedback on for example norepinephrine NE When NE is released into the synapse it feeds back on the a2 receptor causing less NE release from the presynaptic neuron This decreases the effect of NE There are also a2 receptors on the nerve terminal membrane of the post synaptic adrenergic neuron Actions of the a2 receptor include decreased insulin release from the pancreas 19 increased glucagon release from the pancreas contraction of sphincters of the GI tract negative feedback in the neuronal synapses presynaptic inhibition of norepinephrine release in CNS increased platelet aggregation increased blood clotting tendency decreases peripheral vascular resistance a2 agonists see actions above can be used to treat 7 hypertension decrease blood pressure raising actions of the sympathetic nervous system a2 antagonists can be used to treat 7 impotence relax penile smooth muscles and ease blood flow depression enhance mood by increasing norepinephrine secretionb receptors Edit Subtype unspecific b agonists can be used to treat 7 heart failure increase cardiac output acutely in an emergency circulatory shock increase cardiac output thus redistributing blood volume anaphylaxis bronchodilation Subtype unspecific b antagonists beta blockers can be used to treat 7 heart arrhythmia decrease the output of sinus node thus stabilizing heart function coronary artery disease reduce heart rate and hence increasing oxygen supply heart failure prevent sudden death related to this condition 7 which is often caused by ischemias or arrhythmias 21 hyperthyroidism reduce peripheral sympathetic hyper responsiveness migraine reduce number of attacks stage fright reduce tachycardia and tremor glaucoma reduce intraocular pressureb1 receptor Edit Main article Beta 1 adrenergic receptor Actions of the b1 receptor include increase cardiac output by increasing heart rate positive chronotropic effect conduction velocity positive dromotropic effect stroke volume by enhancing contractility positive inotropic effect and rate of relaxation of the myocardium by increasing calcium ion sequestration rate positive lusitropic effect which aids in increasing heart rate increase renin secretion from juxtaglomerular cells of the kidney increase renin secretion from kidney 22 increase ghrelin secretion from the stomach 23 b2 receptor Edit Main article Beta 2 adrenergic receptor Actions of the b2 receptor include smooth muscle relaxation throughout many areas of the body e g in bronchi bronchodilation see salbutamol 19 GI tract decreased motility veins vasodilation of blood vessels especially those to skeletal muscle although this vasodilator effect of norepinephrine is relatively minor and overwhelmed by a adrenoceptor mediated vasoconstriction 24 lipolysis in adipose tissue 25 anabolism in skeletal muscle 26 27 uptake of potassium into cells 28 relax non pregnant uterus relax detrusor urinae muscle of bladder wall dilate arteries to skeletal muscle glycogenolysis and gluconeogenesis stimulates insulin secretion 29 contract sphincters of GI tract thickened secretions from salivary glands 19 inhibit histamine release from mast cells involved in brain immune communication 30 b2 agonists see actions above can be used to treat 7 asthma and COPD reduce bronchial smooth muscle contraction thus dilating the bronchus hyperkalemia increase cellular potassium intake preterm birth reduce uterine smooth muscle contractions 31 b3 receptor Edit Main article Beta 3 adrenergic receptor Actions of the b3 receptor include increase of lipolysis in adipose tissue relax the bladder b3 agonists could theoretically be used as weight loss drugs but are limited by the side effect of tremors See also EditBeta adrenergic receptor kinase Beta adrenergic receptor kinase 2Notes Edit a b There is no a1C receptor There was a subtype known as C but it was found to be identical to one of the previously discovered subtypes To avoid confusion naming was continued with the letter D Before June 1995 a1A was named a1C a1D was named a1A a1D or a1A D 32 References Edit Cannon WB Rosenbluth A 31 May 1933 Studies On Conditions Of Activity In Endocrine Organs XXVI Sympathin E and Sympathin I American Journal of Physiology 104 3 557 574 doi 10 1152 ajplegacy 1933 104 3 557 Dale HH May 1906 On some physiological actions of ergot The Journal of Physiology 34 3 163 206 doi 10 1113 jphysiol 1906 sp001148 PMC 1465771 PMID 16992821 Dale HH Jun 1913 On the action of ergotoxine with special reference to the existence of sympathetic vasodilators The Journal of Physiology 46 3 291 300 doi 10 1113 jphysiol 1913 sp001592 PMC 1420444 PMID 16993202 Marsh DT Pelletier MH Rose CA Feb 1948 The comparative pharmacology of the N alkyl arterenols The Journal of Pharmacology and Experimental Therapeutics 92 2 108 20 PMID 18903395 Ahlquist RP Jun 1948 A study of the adrenotropic receptors The American Journal of Physiology 153 3 586 600 doi 10 1152 ajplegacy 1948 153 3 586 PMID 18882199 S2CID 1518772 Drill VA 1954 Pharmacology in medicine a collaborative textbook New York McGraw Hill a b c d e f g h i j k l m n o Perez Dianne M 2006 The adrenergic receptors in the 21st century Totowa New Jersey Humana Press pp 54 129 134 ISBN 978 1588294234 LCCN 2005008529 OCLC 58729119 Zwieten Van A P 1986 Interaction Between a and b Adrenoceptor Mediated Cardiovascular Effects Journal of Cardiovascular Pharmacology 8 S21 8 doi 10 1097 00005344 198608004 00004 ISSN 0160 2446 PMID 2427848 a b c d e Rang HP Ritter JM Flower RJ Henderson G 2016 Rang and Dale s pharmacology 8th ed United Kingdom Elsevier p 179 ISBN 9780702053627 OCLC 903083639 Prischich Davia Gomila Alexandre M J Milla Navarro Santiago Sanguesa Gemma Diez Alarcia Rebeca Preda Beatrice Matera Carlo Batlle Montserrat Ramirez Laura Giralt Ernest Hernando Jordi Guasch Eduard Meana J Javier de la Villa Pedro Gorostiza Pau 2020 Adrenergic modulation with photochromic ligands Angewandte Chemie International Edition 60 7 3625 3631 doi 10 1002 anie 202010553 hdl 2434 778579 ISSN 1433 7851 PMID 33103317 Tesmer JJ et al 2012 09 21 Paroxetine is a direct inhibitor of g protein coupled receptor kinase 2 and increases myocardial contractility ACS Chemical Biology 7 11 1830 1839 doi 10 1021 cb3003013 ISSN 1554 8929 PMC 3500392 PMID 22882301 Nisoli E Tonello C Landi M Carruba MO 1996 Functional studies of the first selective beta 3 adrenergic receptor antagonist SR 59230A in rat brown adipocytes Molecular Pharmacology 49 1 7 14 PMID 8569714 Elliott J 1997 Alpha adrenoceptors in equine digital veins evidence for the presence of both alpha1 and alpha2 receptors mediating vasoconstriction Journal of Veterinary Pharmacology and Therapeutics 20 4 308 17 doi 10 1046 j 1365 2885 1997 00078 x PMID 9280371 Sagrada A Fargeas MJ Bueno L 1987 Involvement of alpha 1 and alpha 2 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 Smith RS Weitz CJ Araneda RC Aug 2009 Excitatory actions of noradrenaline and metabotropic glutamate receptor activation in granule cells of the accessory olfactory bulb Journal of Neurophysiology 102 2 1103 14 doi 10 1152 jn 91093 2008 PMC 2724365 PMID 19474170 Schmitz JM Graham RM Sagalowsky A Pettinger WA 1981 Renal alpha 1 and alpha 2 adrenergic receptors biochemical and pharmacological correlations The Journal of Pharmacology and Experimental Therapeutics 219 2 400 6 PMID 6270306 Circulation amp Lung Physiology I Archived 2011 07 26 at the Wayback Machine M A S T E R Learning Program UC Davis School of Medicine Moro C Tajouri L Chess Williams R 2013 Adrenoceptor function and expression in bladder urothelium and lamina propria Urology 81 1 211 e1 7 doi 10 1016 j urology 2012 09 011 PMID 23200975 a b c d Fitzpatrick D Purves D Augustine G 2004 Table 20 2 Neuroscience 3rd ed Sunderland Mass Sinauer ISBN 978 0 87893 725 7 Qin K Sethi PR Lambert NA 2008 Abundance and stability of complexes containing inactive G protein coupled receptors and G proteins FASEB Journal 22 8 2920 7 doi 10 1096 fj 08 105775 PMC 2493464 PMID 18434433 Orn S Dickstein K 2002 04 01 How do heart failure patients die European Heart Journal Supplements 4 Suppl D D59 D65 doi 10 1093 oxfordjournals ehjsupp a000770 Kim SM Briggs JP Schnermann J February 2012 Convergence of major physiological stimuli for renin release on the Gs alpha cyclic adenosine monophosphate signaling pathway Clinical and Experimental Nephrology 16 1 17 24 doi 10 1007 s10157 011 0494 1 PMC 3482793 PMID 22124804 Zhao TJ Sakata I Li RL Liang G Richardson JA Brown MS et al Sep 2010 Ghrelin secretion stimulated by beta 1 adrenergic receptors in cultured ghrelinoma cells and in fasted mice Proceedings of the National Academy of Sciences of the United States of America 107 36 15868 73 Bibcode 2010PNAS 10715868Z doi 10 1073 pnas 1011116107 PMC 2936616 PMID 20713709 Klabunde R Adrenergic and Cholinergic Receptors in Blood Vessels Cardiovascular Physiology Retrieved 5 May 2015 Large V Hellstrom L Reynisdottir S et al 1997 Human beta 2 adrenoceptor gene polymorphisms are highly frequent in obesity and associate with altered adipocyte beta 2 adrenoceptor function The Journal of Clinical Investigation 100 12 3005 13 doi 10 1172 JCI119854 PMC 508512 PMID 9399946 Kline WO Panaro FJ Yang H Bodine SC 2007 Rapamycin inhibits the growth and muscle sparing effects of clenbuterol Journal of Applied Physiology 102 2 740 7 doi 10 1152 japplphysiol 00873 2006 PMID 17068216 S2CID 14292004 Kamalakkannan G Petrilli CM George I et al 2008 Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure The Journal of Heart and Lung Transplantation 27 4 457 61 doi 10 1016 j healun 2008 01 013 PMID 18374884 Basic amp Clinical Pharmacology United States of America MCGraw Hill Education 2018 p 148 ISBN 978 1 259 64115 2 Santulli G Lombardi A Sorriento D Anastasio A Del Giudice C Formisano P Beguinot F Trimarco B Miele C Iaccarino G March 2012 Age related impairment in insulin release the essential role of b 2 adrenergic receptor Diabetes 61 3 692 701 doi 10 2337 db11 1027 PMC 3282797 PMID 22315324 Elenkov IJ Wilder RL Chrousos GP Vizi ES December 2000 The sympathetic nerve an integrative interface between two supersystems the brain and the immune system Pharmacological Reviews 52 4 595 638 PMID 11121511 Haas DM Benjamin T Sawyer R Quinney SK 2014 Short term tocolytics for preterm delivery current perspectives International Journal of Women s Health 6 343 9 doi 10 2147 IJWH S44048 PMC 3971910 PMID 24707187 Hieble JP Bylund DB Clarke DE Eikenburg DC Langer SZ Lefkowitz RJ Minneman KP Ruffolo RR June 1995 International Union of Pharmacology X Recommendation for nomenclature of alpha 1 adrenoceptors consensus update Pharmacological Reviews 47 2 267 70 PMID 7568329 Further reading EditRang 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 978 0 443 06911 6 External links EditAlpha receptors illustrated The Adrenergic Receptors Adrenoceptors IUPHAR BPS guide to pharmacology Basic Neurochemistry a and b Adrenergic Receptors Theory of receptor activation Desensitization of b1 receptors Retrieved from https en wikipedia org w index php title Adrenergic receptor amp oldid 1068573449 b receptors, wikipedia, wiki, book,

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