Berotec Mechanism of Action

Pharmacology: Berotec is an effective bronchodilator for use in acute asthma and in other conditions with reversible airway narrowing eg, chronic obstructive bronchitis with or without pulmonary emphysema. After oral administration, Berotec acts within a few mins with a duration of action up to 8 hrs.
Following inhalation of fenoterol hydrobromide in obstructive lung diseases, bronchodilatation occurs within a few minutes. The bronchodilator effect lasts 3-5 hrs.
Fenoterol HBr is a direct-acting sympathomimetic agent, selectively stimulating β₂-receptors in the therapeutic dose range. The stimulation of β₁-receptors comes into effect at a higher dose range (eg, as administered in tocolysis). Occupation of β₂-receptors activates adenyl cyclase via a stimulatory G_s-protein. The increase in cyclic AMP activates protein kinase A which then phosphorylates target proteins in smooth muscle cells. This in turn leads to the phosphorylation of myosin light chain kinase, inhibition of phosphoinositide hydrolysis and the opening of large-conductance calcium-activated potassium channels. There is some evidence that the "maxi-K channel" can be directly activated via the G_s-protein.
Fenoterol relaxes bronchial and vascular smooth muscle and protects against bronchoconstricting stimuli eg, histamine, methacholine, cold air and allergen (early response).
After acute administration, the release of bronchoconstricting and pro-inflammatory mediators from mast cells is inhibited. Furthermore, an increase in mucociliary clearance has been demonstrated after administration of doses of fenoterol (0.6 mg).
Higher plasma concentrations, which are more frequently achieved with oral, or even more so with IV administration, inhibit uterine motility. Also at higher doses, metabolic effects are observed: Lipolysis, glycogenolysis, hyperglycaemia and hypokalaemia, the latter caused by increased K⁺-uptake primarily into skeletal muscle. Beta-adrenergic effects on the heart eg, increase in heart rate and contractility, are caused by the vascular effects of fenoterol, cardiac β₂-receptor stimulation and at supratherapeutic doses, by β₁-receptor stimulation. As with other β-adrenergic agents, QTc prolongation has been reported. For fenoterol MDIs, these events were discrete and observed at doses higher than recommended. However, systemic exposure after adminstration with nebulisers (UDVs, solution for inhalation) might be higher than with recommended MDI doses (see Dosage & Administration). The clinical significance has not been established. Tremor is a more frequently observed effect of β-agonists.
In clinical studies, fenoterol was shown to be highly efficacious in manifest bronchospasm. It prevents bronchoconstriction following exposure to various stimuli eg, exercise cold air and the early response following allergen exposure.