Beta-2 adrenergic receptor
The beta-2 adrenergic receptor (2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor that interacts with (binds) epinephrine, a hormone and neurotransmitter (ligand synonym, adrenaline) whose signaling, via adenylate cyclase stimulation through trimeric Gs proteins, increased cAMP, and downstream L-type calcium channel interaction, mediates physiologic responses such as smooth muscle relaxation and bronchodilation.
The official symbol for the human gene encoding the 2 adrenoreceptor is ADRB2.

# Gene
The ADRB2 gene is intronless. Different polymorphic forms, point mutations, and/or downregulation of this gene are associated with nocturnal asthma, obesity and type 2 diabetes.

# Structure
The 3D crystallographic structure (see figure and links to the right) of the 2-adrenergic receptor has been determined by making a fusion protein with lysozyme to increase the hydrophilic surface area of the protein for crystal contacts.  An alternative method, involving production of a fusion protein with an agonist, supported lipid-bilayer co-crystallization and generation of a 3.5 A resolution structure.

# Mechanism
This receptor is directly associated with one of its ultimate effectors, the class C L-type calcium channel CaV1.2. This receptor-channel complex is coupled to the Gs G protein, which activates adenylyl cyclase, catalysing the formation of cyclic adenosine monophosphate (cAMP) which then activates protein kinase A, and counterbalancing phosphatase PP2A. Protein kinase A then goes on to phosphorylate (and thus inactivate) myosin light-chain kinase, which causes smooth muscle relaxation, accounting for the vasodilatory effects of beta 2 stimulation. The assembly of the signaling complex provides a mechanism that ensures specific and rapid signaling. A two-state biophysical and molecular model has been proposed to account for the pH and REDOX sensitivity of this and other GPCRs.
Beta-2 adrenergic receptors have also been found to couple with Gi, possibly providing a mechanism by which response to ligand is highly localized within cells. In contrast, Beta-1 adrenergic receptors are coupled only to Gs, and stimulation of these results in a more diffuse cellular response. This appears to be mediated by cAMP induced PKA phosphorylation of the receptor.

# Function
Actions of the 2 receptor include:

## Muscular System

## Circulatory system
- Heart muscle contraction
- increase cardiac output (minor degree compared to 1).
Increases heart rate  in sinoatrial node (SA node) (chronotropic effect).
Increases atrial cardiac muscle contractility. (inotropic effect).
Increases contractility and automaticity of ventricular cardiac muscle.
- Increases heart rate  in sinoatrial node (SA node) (chronotropic effect).
- Increases atrial cardiac muscle contractility. (inotropic effect).
- Increases contractility and automaticity of ventricular cardiac muscle.
- Dilate hepatic artery.
- Dilate arterioles to skeletal muscle.

## Eye
In the normal eye, beta-2 stimulation by salbutamol increases intraocular pressure via net:
- Increase in production of aqueous humour by the ciliary process,
- Subsequent increased pressure-dependent uveoscleral outflow of humour, despite reduced drainage of humour via the Canal of Schlemm.
In glaucoma, drainage is reduced ( open-angle glaucoma) or blocked completely (closed-angle glaucoma). In such cases, beta-2 stimulation with its consequent increase in humour production is highly contra-indicated, and conversely, a topical beta-2 antagonist such as timolol may be employed.

## Digestive system
- Glycogenolysis and gluconeogenesis in liver.
- Glycogenolysis and lactate release in skeletal muscle.
- Contract sphincters of Gastrointestinal tract.
- Thickened secretions from salivary glands.
- Insulin and glucagon secretion from pancreas. 

## Other
- Inhibit histamine-release from mast cells.
- Increase protein content of secretions from lacrimal glands.
- Receptor also present in cerebellum.
- Bronchiole dilation (targeted while treating asthma attacks)
- Involved in brain - immune - communication 

# Agonists

## Spasmolytics used in asthma and COPD
- Short-acting 2 agonists (SABA)
bitolterol
fenoterol
hexoprenaline
isoprenaline (INN) or isoproterenol (USAN)
levosalbutamol (INN) or levalbuterol (USAN)
-rciprenaline (INN) or metaproterenol (USAN)
pirbuterol
procaterol
salbutamol (INN) or albuterol (USAN)
terbutaline
- bitolterol
- fenoterol
- hexoprenaline
- isoprenaline (INN) or isoproterenol (USAN)
- levosalbutamol (INN) or levalbuterol (USAN)
- orciprenaline (INN) or metaproterenol (USAN)
- pirbuterol
- procaterol
- salbutamol (INN) or albuterol (USAN)
- terbutaline
- Long-acting 2 agonists (LABA)
arformoterol (some consider it to be an ultra-LABA)
bambuterol
clenbuterol
formoterol
salmeterol
- arformoterol (some consider it to be an ultra-LABA)
- bambuterol
- clenbuterol
- formoterol
- salmeterol
- Ultra-long-acting 2 agonists (ultra-LABA)
carmoterol
indacaterol
milveterol (GSK 159797)
-lodaterol
vilanterol (GSK 642444)
- carmoterol
- indacaterol
- milveterol (GSK 159797)
- olodaterol
- vilanterol (GSK 642444)

## Tocolytic agents
- Short-acting 2 agonists (SABA)
fenoterol
hexoprenaline
isoxsuprine
ritodrine
salbutamol (INN) or albuterol (USAN)
terbutaline
- fenoterol
- hexoprenaline
- isoxsuprine
- ritodrine
- salbutamol (INN) or albuterol (USAN)
- terbutaline

## 2 agonists used for other purposes
- zilpaterol

# Antagonists
(Beta blockers)
- butoxamine*
- First generation (non-selective) -blockers
- ICI-118,551*
- Propranolol
- denotes selective antagonist to the receptor.

# Interactions
Beta-2 adrenergic receptor has been shown to interact with:
- AKAP12,
- OPRD1,
- Grb2,
- SNX27  and
- SLC9A3R1.