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Image:Adrenaline.svg The adrenergic receptors (or adrenoceptors) are a class of G protein-coupled receptors that are targets of the catecholamines. Adrenergic receptors specifically bind their endogenous ligands, the catecholamines adrenaline and noradrenaline (also called epinephrine and norepinephrine in the USA), and are activated by these.

Many cells possess these receptors, and the binding of an agonist will generally cause the cell to respond in a fight-or-flight manner. For instance, the heart rate will increase and the pupils will dilate, energy will be mobilized, and blood flow diverted from other organs to skeletal muscle.

Contents 1 Subtypes of adrenergic receptors 2 Comparison 3 Diagram 4 References 5 External links

[edit] Subtypes of adrenergic receptors

There are several types of adrenergic receptors, but there are two main groups: α-Adrenergic and β-Adrenergic.

• α receptors bind norepinephrine and epinephrine, though norepinephrine has higher affinity. Phenylephrine is a selective agonist of the α receptor.
• β receptors are linked to G_s proteins, which in turn are linked to adenylyl 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.

[edit] Comparison

Receptor type	Agonist potency order	Location	Mechanism / Action	Agonists	Antagonists
α1: ADRA1A, ADRA1B, ADRA1D	norepinephrine ≥ epinephrine >> isoprenaline	smooth muscle	Hormone binding activates the associated Gq protein, which is linked to phospholipase C (PLC). PLC produces IP3, which causes a rise in intracellular calcium levels, and diacylglycerol. Elevated calcium and diacylglycerol activate protein kinase C, which mediates the downstream, intracellular effects of the hormone. In blood vessels the principal effect is vasoconstriction. Blood vessels with α1 receptors are present in the skin and the gastrointestinal system, and during the fight-or-flight response vasoconstriction results in the decreased blood flow to these organs. This accounts for an individual's skin appearing pale when frightened. In the GI tract, the effect is relaxation.	norepinephrine phenylephrine	(Alpha blockers) phenoxybenzamine phentolamine prazosin tamsulosin terazosin
α2: ADRA2A, ADRA2B, ADRA2C	epinephrine > noradrenaline >> isoprenaline	pre- and postsynaptic nerve terminals	Each subtype is linked to a Gi protein, which works in opposition to Gs proteins, suppressing adenylate cyclase activity with a consequent decrease in intracellular cAMP levels. Mediates synaptic transmission.	clonidine lofexidine xylazine	(Alpha blockers) yohimbine
β1: ADRB1	isoprenaline > norepinephrine > epinephrine	heart and cerebral cortex	adenylate cyclase active, cAMP up In heart, agonists enhance myocardial contractility and increase heart rate.	norepinephrine isoproterenol dobutamine	(Beta blockers) metoprolol
β2: ADRB2	isoprenaline > epinephrine > norepinephrine	lung, smooth muscle, cerebellum	adenylate cyclase active, cAMP up In lung, agonists cause bronchiole dilation. Agonists can be useful in treating asthma. In smooth muscle, relaxes walls.	(Short/long) albuterol bitolterol mesylate formoterol isoproterenol levalbuterol metaproterenol salmeterol terbutaline	(Beta blockers) butoxamine propranolol
β3: ADRB3	isoprenaline > norepinephrine = epinephrine	adipose tissue	adenylate cyclase active, cAMP up Agonists enhance lipolysis.	?	(Beta blockers)  ?

The absence of "ADRA1C" is intentional. At one time, there was a subtype known as C, but was found to be one of the previously discovered subtypes. To avoid confusion, it was decided that there would never be a C subtype again and so if any new subtypes were discovered, naming would start with E.

[edit] Diagram

Image:Adrenozeptor-Signaltransduktion.jpg Image:G protein signal transduction (epinephrin pathway).png

[edit] References