A patient with neurogenic bladder is treated with mirabegron. The mechanism of action of mirabegron differs from older agents used for overactive bladder in that it:

• A Activates beta-3 adrenergic receptors on detrusor smooth muscle, promoting relaxation during the storage phase ✓
• B Blocks muscarinic M3 receptors on detrusor muscle, reducing urgency
• C Blocks alpha-1A adrenergic receptors on the bladder neck, reducing outlet resistance
• D Inhibits vanilloid TRPV1 channels on bladder afferents

Explanation

Mirabegron is the first-in-class beta-3 adrenoceptor agonist approved for overactive bladder. The bladder detrusor is predominantly beta-3 subtype (not beta-2). Beta-3 activation causes cAMP-mediated relaxation of detrusor smooth muscle during the filling/storage phase, increasing bladder capacity without blocking muscarinic receptors. Unlike anticholinergics (oxybutynin, solifenacin), mirabegron avoids dry mouth, constipation, and cognitive effects in elderly, making it preferred in high-risk populations.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.