β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:

Isoprenaline > Adrenaline > Noradrenaline

Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β₁, β₂, and β₃ subtypes.

β₁-adrenoceptors: β₁-adrenoceptors have equal affinities for adrenaline and noradrenaline. They are located postsynaptically in cardiac and brain tissue, lipocytes, and presynaptically on cholinergic and adrenergic nerve terminals, as well as renal cells. Stimulation of β₁-adrenoceptors causes increased myocardial contractility, tachycardia, lipolysis, and renin production.

β₂-adrenoceptors: β₂ receptors have a higher affinity for adrenaline and are located postsynaptically in the cardiac and smooth muscles of blood vessels. Their stimulation causes bronchodilation, vasodilation, decreased peripheral resistance, increased glucagon release and glycogenolysis in the liver and muscles, and uterine relaxation in females.

β₃-adrenoceptors: β₃ receptors show higher sensitivity to noradrenaline and are located postsynaptically on the heart and lipocytes and regulate lipolysis along with β₁-adrenoceptors and metabolic activity.