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The beta-2 adrenergic receptor (β 2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor that binds epinephrine (adrenaline), a hormone and neurotransmitter whose signaling, via adenylate cyclase stimulation through trimeric G s proteins, increases cAMP, and, via downstream L-type calcium channel interaction, mediates physiologic responses such as smooth ...
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 (β 2) antagonists and alpha-2 (α 2) agonists, which are used to treat high ...
Beta 2-adrenergic agonists, also known as adrenergic β 2 receptor agonists, are a class of drugs that act on the β 2 adrenergic receptor. Like other β adrenergic agonists, they cause smooth muscle relaxation. β 2 adrenergic agonists' effects on smooth muscle cause dilation of bronchial passages, vasodilation in muscle and liver, relaxation ...
G-protein-coupled receptor kinase 2 (GRK2) is an enzyme that in humans is encoded by the ADRBK1 gene. [5] GRK2 was initially called Beta-adrenergic receptor kinase (βARK or βARK1), and is a member of the G protein-coupled receptor kinase subfamily of the Ser/Thr protein kinases that is most highly similar to GRK3(βARK2).
Direct-acting analog binds the β-adrenergic receptors directly and generates sympathetic response. Indirect-acting analog causes agonistic effect but without a direct binding to the β-adrenergic receptor, for example, by promoting release of norepinephrine (NE) from the presynaptic terminal or by inhibiting reuptake of released NE. [14]
The three types present are: alpha-1, alpha-2 and beta-2 adrenergic receptors|. The main endogenous agonist of these cell receptors is norepinephrine (NE). The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: alpha-1 receptors.
Beta-2 blockers stops the above-mentioned signaling pathway, (formation of cAMP, release of protein kinase A, reduction of intracellular calcium level) by blocking the receptor. Remarks: It has to be noted that alpha-1 receptor has an opposite action when it is compared with beta 2 receptor.
Activation of β 2 receptors induces smooth muscle relaxation in the lungs, gastrointestinal tract, uterus, and various blood vessels. Increased heart rate and heart muscle contraction are associated with the β1 receptors; however, β 2 cause vasodilation in the myocardium. [citation needed] β3 receptors are mainly located in adipose tissue. [5]