Acetylcholine (ACh), a common neurotransmitter in the human, acts in the brain at the neuromuscular junction and throughout the autonomic nervous system. Cholinergic receptors have been separated into two main groups: nicotonic (present at the neuromuscular junction) and muscarinic (present at all ganglia of the autonomic nervous system and postsynaptically in the parasympathetic nervous system).
Anticholinergic medicines act at muscarinic sites. The first anticholinergic drugs were extracts of belladonna plants, which were used for centuries for their antimotility and antisecretory properties. These drugs generally are ineffective blockers of ACh at nicotinic receptors and cause neuromuscular blockade only at excessive doses.
Because antimuscarinic medications block the effect of the parasympathetic nervous system, they affect the gastrointestinal (GI) tract. In general, the parasympathetic nervous system stimulates the GI system. Cholinergic impulses cause increased tone and motility of the stomach and intestines and increased secretion of gastric and intestinal fluids. Exocrine pancreatic secretion and gallbladder contraction also are stimulated by cholinergic activity. Anticholinergics reverse these responses.
The prototypical anticholinergic, atropine, decreases output of gastric, intestinal, and pancreatic secretions; decreases motility and tone of the GI tract; and relaxes the gallbladder. Atropine not only interferes with cholinergic activity in the GI tract, it affects the entire body increasing heart rate, depressing salivary and bronchial secretion, decreasing sweating, dilating the pupils, inhibiting accommodation, inhibiting micturition, and causing constipation.
