ganglionic blocker
A ganglionic blocker shuts down the relay stations of the autonomic nervous system. Both the sympathetic and parasympathetic pathways pass through clusters of nerve cells called ganglia, and these drugs jam the connection there, so neither branch can deliver its message to the organs downstream.
They work at the neuronal nicotinic acetylcholine receptor in autonomic ganglia, blocking the transmission from preganglionic to postganglionic neurons. Because every autonomic signal must cross a ganglion, blocking it affects both divisions at once. The result on any organ depends on which branch normally dominates there: blocking the sympathetically dominated vessels causes vasodilation and a fall in blood pressure, while blocking the parasympathetically dominated gut and bladder causes constipation and retention.
Historically, drugs like hexamethonium and trimethaphan were among the first effective treatments for severe high blood pressure. Today they are essentially obsolete because their effects are so widespread and unpredictable, but they remain a clear teaching model of autonomic physiology.
Trimethaphan was once infused to produce deliberate low blood pressure during certain operations, by blocking sympathetic ganglia that maintain vascular tone.
A historic drug for controlled hypotension.
Both ganglionic blockers and neuromuscular blockers act on nicotinic receptors, but on different subtypes: ganglionic blockers hit the neuronal receptor in ganglia, while neuromuscular blockers hit the muscle receptor at the neuromuscular junction.