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Pharmacology of Airway Control Quiz
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What is the primary mechanism of action of short-acting beta2 agonists such as salbutamol in asthma?
- A Competitive antagonism at histamine H1 receptors in the bronchial tree You picked ✕
- B Activation of Gi-coupled beta2 receptors, decreasing intracellular cAMP You picked ✕
- C Inhibition of phosphodiesterase, preventing breakdown of cAMP in airway smooth muscle You picked ✕
- D Blockade of muscarinic M3 receptors on airway smooth muscle, reducing bronchoconstriction You picked ✕
- E Activation of Gs-coupled beta2 receptors, increasing cAMP You picked ✓
Correct!
Incorrect
The answer is E: Activation of Gs-coupled beta2 receptors, increasing cAMP
Explanation
Why E is correct
See Short-Acting β2 Agonists (SABAs). Option E is correct because short-acting beta2 agonists (SABAs) such as salbutamol and terbutaline stimulate Gs-coupled beta2 receptors on airway smooth muscle. A G-protein-coupled receptor passes its message through a G protein inside the cell, and the Gs type stimulates the enzyme adenylyl cyclase. This raises intracellular cyclic AMP (cAMP), which causes the smooth muscle to relax, so the airways widen and bronchodilation follows. Onset is within minutes and the effect lasts 4 to 6 hours, which suits their use as relievers for symptoms, in acute exacerbations (often by nebuliser) and before exercise. Side effects come mainly from beta2 stimulation in other tissues: tremor from skeletal muscle, palpitations and tachycardia, hypokalaemia (beta2 stimulation drives potassium into cells, which is why nebulised salbutamol is used in hyperkalaemia), hyperglycaemia and, at high doses, lactic acidosis. Frequent SABA use is a marker of poor asthma control. A memory aid: beta2 plus Gs means more cAMP and a relaxed airway.
- Receptor: short-acting beta2 agonists stimulate Gs-coupled beta2 receptors on airway smooth muscle.
- Pathway: Gs activates adenylyl cyclase, which raises cAMP and relaxes the muscle.
- Timing: onset within minutes and effect lasting 4 to 6 hours, so they are relievers.
- Side effects: tremor, tachycardia and hypokalaemia from beta2 stimulation in other tissues.
Why the other options are incorrect
- A. Competitive antagonism at histamine H1 receptors in the bronchial tree: H1 antagonists block histamine-mediated allergic effects and do not produce direct bronchodilation. Salbutamol is not an antihistamine. Your answer
- B. Activation of Gi-coupled beta2 receptors, decreasing intracellular cAMP: Beta2 receptors are coupled to Gs, not Gi, and their activation increases rather than decreases cAMP. A fall in cAMP would narrow the airways. Your answer
- C. Inhibition of phosphodiesterase, preventing breakdown of cAMP in airway smooth muscle: Phosphodiesterase inhibition is the mechanism of theophylline, which gives a slower, weaker bronchodilator effect than salbutamol. Salbutamol raises cAMP by increasing its production. Your answer
- D. Blockade of muscarinic M3 receptors on airway smooth muscle, reducing bronchoconstriction: Blocking muscarinic M3 receptors is the action of antimuscarinic drugs such as ipratropium. Salbutamol acts on beta2 receptors. Your answer
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More questions from this set. Start the quiz to answer them and see each explanation.
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1
A 19-year-old student with asthma uses salbutamol several times most days and wakes with wheeze twice a week. He takes no preventer treatment. After his inhaler technique and adherence have been checked, which treatment strategy best addresses his poor control?
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2
A 19-year-old university student with newly diagnosed persistent asthma is started on a regular inhaled corticosteroid. Which of the following best describes the primary mechanism by which inhaled corticosteroids improve asthma control?
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