Autonomic pharmacology
Practice questions with explanations

A. Dexmedetomidine produces sedation without significant respiratory depression, as it acts through central alpha-2 receptors rather than GABA

Reducing central sympathetic outflow produces a state resembling natural sleep from which patients rouse, and it spares respiratory drive, which suits weaning from ventilation. Bradycardia and hypotension are the main adverse effects. Clonidine shares the mechanism and is used for withdrawal states and as an adjunct in pain management.

B. Beta-2 adrenoceptor

Beta-2 adrenoceptors on airway smooth muscle couple to Gs, raise cyclic AMP and relax the muscle. Salbutamol is selective for them, though selectivity is relative and the tremor and tachycardia seen at high doses come from beta-2 receptors in skeletal muscle and from spillover onto cardiac receptors. Beta-1 stimulation acts on the heart, alpha-1 constricts vessels, and blocking M3 receptors is how ipratropium produces bronchodilation instead.

D. Bethanechol

Bethanechol is a choline ester resistant to acetylcholinesterase, acting directly on muscarinic receptors in the detrusor to promote emptying. Neostigmine raises acetylcholine indirectly by inhibiting the enzyme and acts at nicotinic sites as well. Oxybutynin does the opposite by blocking muscarinic receptors, and phenylephrine is an alpha-1 agonist that would increase outflow resistance.