In the classic Furchgott experiments, intra-arterial acetylcholine caused vasodilation even though most blood vessels receive no parasympathetic innervation. The correct mechanism is:

• A Acetylcholine stimulates endothelial M3 receptors, releasing nitric oxide that relaxes underlying smooth muscle ✓
• B Acetylcholine acts on vascular smooth muscle M3 receptors to hyperpolarize the cell
• C Acetylcholine releases stored norepinephrine from sympathetic terminals, which then activates beta-2 receptors
• D Acetylcholine directly opens potassium channels on vascular smooth muscle independent of any receptor

Explanation

Endothelial cells express muscarinic M3 receptors even though parasympathetic nerves do not reach most vessels. Acetylcholine acting there raises endothelial calcium and releases nitric oxide, which diffuses to smooth muscle and raises cGMP, causing dilation. The response disappears when the endothelium is mechanically removed, the observation that won Furchgott the Nobel Prize. Option B fails because vascular smooth muscle M3 receptors would contract, not relax.

Reference: Ganong Review of Medical Physiology, 26th ed.

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