Long-Acting Beta-Agonist

A) Long-acting beta agonist: Beta-agonists (Beta2-agonists) are the medications that affect smooth muscles surrounding airways.1 In an irritated state of lung, muscles around the airways are constricted; these kinds of drugs can influence these muscles and make them relaxed, which brings about widening of airway and leads to comfortable breath (“easier breathing”1).1 They are categorized into two subtypes according to their duration time of action, including long-acting and short-acting. They can be administrated in different types; however, the most common type of their administration is in inhalation form. The other types such as pills, tablets, etc. may have more side effects.1
Regarding COPD treatment, beta2-agonists are administrated
B) The crucial mechanism of β2-agonists is inducing the β2-adrenergic receptors, which leads to smooth muscle relaxation and consequently causes the airway to be relaxed (brochodilation).3,9-11 Regarding this mechanism, briefly, airway smooth muscles have a lot of β2-adrenergic receptors (β2-AR) and β2-agonist acts by binding to these receptors.3,9-11 This binding leads to activation of intracellular coupling stimulatory G proteins that binds to guanosine triphosphate (GTP) with activation of the adenylate cyclase.3,9-11 The interaction between the receptors and G proteins causes activation of intracellular cyclic adenosine monophosphate (cAMP) and enhances its level.3,9-12 This leads to activation protein kinase A (PKA), which phosphorylates a variety of targets that cause relaxing and mediating smooth muscle as well as bronchodilation effect.3,9-12 However, these targets are not known meticulously, it is assumed that they may involve myosin light chain kinase and calcium dependent potassium channels.3,10,13 Therefore, it can be concluded that activation of β2-adrenergic receptors affects directly in bronchodilation.3,9 Furthermore, beta2-agonists may affect parasympathetic nervous system and modulate it by impressing presynaptic β2 receptors at parasympathetic ganglia.3 Apart from the main mechanism of action that was described above (bronchodilation), other mechanisms that lead to a reduction in airway obstruction, in theory, include the effect of this kind of drug on
As well as this, a decrease in all component scores of SGRQ demonstrated an improvement in health status in both groups of moderate and severe COPD patients and also with both doses of indacaterol. Strikingly, the symptom scores were statistically significant in patients with severe COPD with 300 μg doses of indacaterol rather than placebo (p < 0.01). The impact scores were taken into consideration statistically significant (p < 0.05) with both indacaterol doses in severe COPD compared with