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A Beta-2 adrenergic antagonist (β 2-adrenoceptor antagonist) is an adrenergic antagonist which blocks the beta-2 adrenergic receptors of cells, with either high specificity (an antagonist which is selective for β 2 adrenoceptors) like Butaxamine and ICI-118,551, or non-specifically (an antagonist for β 2 and for β 1 or β 3 adrenoceptors) like the non-selective betablocker Propranolol.
Figure 1: The chemical structure of dichloroisoprenaline or dichloroisoproterenol (), abbreviated DCI — the first β-blocker to be developed. β adrenergic receptor antagonists (also called beta-blockers or β-blockers) were initially developed in the 1960s, for the treatment of angina pectoris but are now also used for hypertension, congestive heart failure and certain arrhythmias. [1]
Beta 2 blockers cease action of beta-2 receptor by blocking the receptor and preventing it from being activated. [6] Similar to beta-1 receptor, the activated beta-2 receptor will lead to the detach of alpha subunit of Gs protein and attachment of adenylate cyclase. [6] Adenosine triphosphate(ATP), is then catalyzed to form cAMP.
Beta blockers vary in their lipophilicity (fat solubility) and in turn in their ability to cross the blood–brain barrier and exert effects in the central nervous system. [76] Beta blockers with greater blood–brain barrier permeability can have both neuropsychiatric therapeutic benefits and side effects, as well as adverse cognitive effects ...
Beta blockers exert their pharmacological effect, decreased heart rate, by binding to and competitively antagonising a type of receptor called beta adrenoceptors. [1] In pharmacology, the term mechanism of action (MOA) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect. [2]
It is also a adrenergic blocker with no partial agonist action and minimal membrane stabilizing activity. [2] Being selective for beta 1 receptors, it typically has fewer systemic side effects than non-selective beta-blockers, for example, not causing bronchospasm (mediated by beta 2 receptors) as timolol may.
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.
Selective beta 2 blockers impede the activity of beta 2 adrenergic receptors that are mainly situated in the airway smooth muscle of the lungs. [5] By inhibiting the beta 2 receptor-mediated smooth muscle relaxation, beta 2 blockers narrow airways and blood vessels. [5]