Albuterol is a moderately selective beta2-receptor agonist. Albuterol is a racemic mixture of R- and S-isomers, and is widely used as a bronchodilator. It is indicated for the management of asthma exacerbations or other chronic obstructive airway diseases. It is similar in structure to terbutaline, but exhibits less cardiac stimulation and more prolonged bronchodilation than isoproterenol or metaproterenol. Albuterol was originally approved by the FDA in 1981. Outside the US, albuterol is referred to as salbutamol. The R-isomer of albuterol is commercially available as levalbuterol nebulizer solution

Albuterol is a moderately selective beta2-adrenergic agonist that stimulates receptors of the smooth muscle in the lungs, uterus, and vasculature supplying skeletal muscle. Albuterol is racemic beta-agonist, comprised of an equal mixture of R- and S-isomers. The R-isomer, known as levalbuterol, is primarily responsible for bronchodilation. Although not confirmed during clinical trials, the S-isomer of albuterol has bronchoconstrictive properties in animal models.

Intracellularly, the actions of albuterol are mediated by cyclic AMP, the production of which is augmented by beta2-stimulation. Albuterol is believed to work by activating adenylate cyclase, the enzyme responsible for generating cyclic AMP, an intracellular mediator. Increased cyclic AMP leads to activation of protein kinase A, which inhibits phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation. The net result of beta2-receptor agonism in the lungs is relaxation of bronchial and tracheal smooth muscles, which in turn relieves bronchospasm, reduces airway resistance, facilitates mucous drainage, and increases vital capacity.

Albuterol can also inhibit the degranulation and subsequent release of inflammatory autocoids from mast cells. Stimulation of beta2-receptors on peripheral vascular smooth muscle can cause vasodilation and a modest decrease in diastolic blood pressure. Beta2-adrenergic stimulation also results in intracellular accumulation of serum potassium, possibly due to stimulation of the Na/K ATPase pump, leading to moderate degrees of hypokalemia.

Albuterol can be administered as oral tablets or oral solution, but is more commonly administered by oral inhalation. Following oral inhalation, albuterol is absorbed over several hours from the respiratory tract. It is postulated from studies with other inhaled bronchodilators that most of an albuterol inhaled dose (approximately 90%) is actually swallowed and absorbed through the GI tract. Onset of bronchodilation occurs within 5–15 minutes after oral inhalation, peaks in 0.5–2 hours, and lasts 2–6 hours. Administration via nebulization does not appear to significantly alter the pharmacokinetics of albuterol. When administered orally, albuterol is well absorbed through the GI tract. Onset of action begins within 30 minutes, peak levels are reached in 2–3 hours, and duration of action is 4–6 hours for the conventional-release tablets and 8–12 hours for the sustained-release product.

Albuterol crosses the blood-brain barrier and may cross the placenta. The liver metabolizes albuterol extensively to inactive compounds. Excretion of albuterol occurs through the urine and feces. After oral inhalation, 80–100% of a dose is excreted via the kidneys within 72 hours; up to 10% may be eliminated in feces. After oral administration, 75% of a dose is excreted in urine within 72 hours as metabolites; 4% may be found in feces. The elimination half-life of albuterol ranges from 2.7–6 hours, with orally administered albuterol having a shorter half-life than the inhaled product.
 
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