Trimetaphan's mechanism: direct

• A. Vasodilation and ganglionic blockade
• B. Beta-blockade
• C. Calcium channel blockade
• D. Platelet inhibition

Answer: (D)

The key idea is that trimetaphan acts as a direct autonomic ganglionic blocker by antagonizing nicotinic acetylcholine receptors in autonomic ganglia (the Nn receptors). Blocking these receptors stops transmission in both sympathetic and parasympathetic pathways, so postganglionic autonomic output to organs is largely knocked out.

Because sympathetic outflow to the vasculature is interrupted, vascular tone falls and vessels dilate, producing vasodilation and hypotension. The heart’s rate and rhythm are affected by losing parasympathetic (and sympathetic) inputs, so heart rate changes can be variable, but the hallmark mechanism is the direct blockade at autonomic ganglia, not actions on beta receptors, calcium channels, or platelets.

Beta-blockade targets beta-adrenergic receptors, calcium channel blockers inhibit calcium influx in smooth and cardiac muscle, and platelet inhibition refers to anti-platelet mechanisms. None of those describe the direct nicotinic ganglionic blockade that trimetaphan produces.