Mechanism of action Activation of β2 adrenergic
receptors on airway smooth muscle leads to the activation of
adenylate cyclase and to an increase in the intracellular concentration of
3',5'-cyclic adenosine monophosphate (cyclic AMP). The increase in cyclic AMP is associated with the activation of protein
kinase A, which in turn, inhibits the
phosphorylation of
myosin and lowers intracellular ionic calcium concentrations, resulting in muscle relaxation. Levosalbutamol relaxes the smooth muscles of all airways, from the
trachea to the terminal bronchioles. Increased cyclic AMP concentrations are also associated with the inhibition of the release of mediators from mast cells in the airways. Levosalbutamol acts as a functional
agonist that relaxes the airway irrespective of the spasmogen involved, thereby protecting against all
bronchoconstrictor challenges. While it is recognized that β2 adrenergic receptors are the predominant receptors on bronchial smooth muscle, data indicate that there are beta receptors in the human heart, 10–50% of which are β2 adrenergic receptors. The precise function of these receptors has not been established. However, all β-adrenergic agonist drugs can produce a significant
cardiovascular effect in some patients, as measured by pulse rate, blood pressure, and restlessness symptoms, and/or
electrocardiographic (ECG). Levosalbutamol and
salbutamol do not
racemize significantly before being eliminated from the human body.
Enantiomerically pure levosalbutamol is preferred over racemic
salbutamol in most cases, because the other
optical isomer (S-salbutamol) has some negative side-effects. == Society and culture ==