Hexamethonium Bromide (Hexamethonium Dibromide), a specific antagonist of neuronal-type nicotinic AChR in ganglia, is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier.

Hexamethonium Bromide is effective against Ach and carbachol (CCh) on the amplitude of endplate responses of rat omohyoid muscle with EC50 of 300 μM and 100 μM, respectively. Hexamethonium Bromide (50-200 μM) causes an increase in the amplitude of nerve-evoked endplate currents (e.p.cs) recorded in the presence of 0.6 μM tubocurarine. Hexamethonium Bromide is also a weak inhibitor of acetylcholinesterase activity in rat muscle homogenates with EC50 of 1.5 mM. [1] Hexamethonium Bromide (200 μM) decreases the time constant of decay of both endplate currents (e.p.cs) (by ~25%) and miniature endplate currents (m.e.p.cs) (by ~20%) in the rat hemi-diaphragm muscle. At low frequencies of stimulation (0.5-2 Hz), Hexamethonium Bromide (200 μM) increases e.p.c. quantal content by 30-40%. [2]