Theophylline's bronchodilatory mechanism at therapeutic concentrations is PRIMARILY through:
- A Non-selective inhibition of phosphodiesterase (PDE) III and IV, raising cAMP and cGMP levels in bronchial smooth muscle ✓
- B Competitive antagonism at adenosine A1 and A2 receptors in airways, preventing bronchoconstriction
- C Inhibition of histone deacetylase-2 (HDAC2), enhancing corticosteroid anti-inflammatory efficacy
- D Activation of beta-2 adrenergic receptors, mimicking sympathomimetic bronchodilation
Correct answer: A. Non-selective inhibition of phosphodiesterase (PDE) III and IV, raising cAMP and cGMP levels in bronchial smooth muscle
Explanation
At therapeutic concentrations (10–20 mg/L), theophylline primarily inhibits PDE III and IV (cyclic AMP-specific PDE), raising intracellular cAMP in bronchial smooth muscle cells, leading to relaxation and bronchodilation. Adenosine antagonism (option B) occurs at sub-therapeutic concentrations and contributes to side effects (tachycardia, seizures) rather than primary bronchodilation. HDAC2 activation (option C) is a low-dose anti-inflammatory effect. Theophylline is a methylxanthine, not an adrenergic agonist.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.