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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 (β 2) antagonists and alpha-2 (α 2) agonists, which are used to treat high ...
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 ...
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]
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 ...
An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors.The five main categories of adrenergic receptors are: α 1, α 2, β 1, β 2, and β 3, although there are more subtypes, and agonists vary in specificity between these receptors, and may be classified respectively.
The binding to these receptors by catecholamines will generally stimulate the sympathetic nervous system, the arm of the autonomic nervous system responsible for the fight-or-flight response. Adrenergic receptor autoantibodies are autoantibodies (antibodies directed against a person's own protein) targeting adrenergic receptors.
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
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]