Metaterol
{{Drugbox | verifiedfields = changed | verifiedrevid = 477002123 | IUPAC_name = (1R,2S)-2-[[3-(tert-butylamino)-2-hydroxypropyl]amino]-1-phenylethanol | image = Metaterol.svg | image_size = 200px | image_alt = Structural formula of Metaterol }}
Metaterol is a beta-adrenergic agonist that is primarily used in the treatment of asthma and other conditions involving bronchoconstriction. It functions by stimulating beta-2 adrenergic receptors in the bronchial smooth muscle, leading to muscle relaxation and bronchodilation.
Pharmacology[edit]
Metaterol is classified as a beta-2 adrenergic receptor agonist. These receptors are part of the adrenergic receptor family, which are G protein-coupled receptors that respond to epinephrine and norepinephrine. Activation of beta-2 receptors in the lungs results in the relaxation of bronchial smooth muscle, which helps to alleviate symptoms of bronchoconstriction such as wheezing and shortness of breath.
Mechanism of Action[edit]

Metaterol binds to beta-2 adrenergic receptors on the surface of bronchial smooth muscle cells. This binding activates adenylate cyclase, an enzyme that converts ATP to cAMP (cyclic adenosine monophosphate). Increased levels of cAMP lead to the activation of protein kinase A (PKA), which phosphorylates target proteins that result in muscle relaxation and bronchodilation.
Clinical Use[edit]
Metaterol is used in the management of asthma and chronic obstructive pulmonary disease (COPD). It is particularly effective in providing relief from acute bronchospasm. The drug is typically administered via inhalation, which allows for direct delivery to the lungs and rapid onset of action.
Side Effects[edit]
Common side effects of Metaterol include tremor, nervousness, and tachycardia. These effects are generally mild and result from the systemic absorption of the drug, which can stimulate beta-adrenergic receptors in other tissues. In rare cases, more severe cardiovascular effects can occur, particularly in patients with pre-existing heart conditions.
Related Pages[edit]
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