ATC Group: N07A Parasympathomimetics

Ambenonium (as ambenonium dichloride) is a cholinesterase inhibitor used in the management of myasthenia gravis. Ambenonium exerts its actions against myasthenia gravis by competitive reversible inhibition of acetylcholinesterase, the enzyme responsible for the hydrolysis of acetylcholine.

Bethanechol chloride, a cholinergic agent, is a synthetic ester which is structurally and pharmacologically related to acetylcholine. Bethanechol chloride acts principally by producing the effects of stimulation of the parasympathetic nervous system. It stimulates gastric motility, increases gastric tone and often restores impaired rhythmic peristalsis. It is not destroyed by cholinesterase and its effects are more prolonged than those of acetylcholine.

Carbachol is a potent cholinergic (parasympathomimetic) agent which produces constriction of the iris and ciliary body resulting in reduction in intraocular pressure (IOP).

Cevimeline is a cholinergic agonist which binds to muscarinic receptors. Muscarinic agonists in sufficient dosage can increase secretion of exocrine glands, such as salivary and sweat glands and increase tone of the smooth muscle in the gastrointestinal and urinary tracts.

Neostigmine inhibits cholinesterase activity and prolongs and intensifies the muscarinic and nicotinic effects of acetylcholine. The anticholinesterase actions of neostigmine are reversible. It is used mainly for its action on skeletal muscle and less frequently to increase the activity of smooth muscle.

Pilocarpine is a cholinergic parasympathomimetic agent exerting a broad spectrum of pharmacologic effects with predominant muscarinic action. Pilocarpine, in appropriate dosage, can increase secretion by exocrine glands such as the sweat, salivary, lacrimal, gastric, pancreatic and intestinal glands and the mucous cells of the respiratory tract.

Pyridostigmine is an antagonist to cholinesterase, the enzyme which normally destroys acetylcholine. The action of pyridostigmine can briefly be described, therefore, as the potentiation of naturally occurring acetylcholine.