Competitively inhibits acetylcholine or other cholinergic stimuli at autonomic effectors innervated by postganglionic cholinergic nerves and, to a lesser extent, on smooth muscles that lack cholinergic innervation. At usual doses, principally antagonizes cholinergic stimuli at muscarinic receptors and has little or no effect on cholinergic stimuli at nicotinic receptors.
Antimuscarinics also have been referred to as anticholinergics (cholinergic blocking agents), but this term is appropriate only when it describes the antagonism of cholinergic stimuli at any cholinergic receptor, whether muscarinic or nicotinic.
Also have been referred to as parasympatholytics because the antagonized functions principally are under the parasympathetic division of the nervous system.
Receptors at various sites are not equally sensitive to inhibition of muscarinic effects. Relative sensitivity of physiologic functions (proceeding from the most sensitive) is as follows: secretions of the salivary, bronchial, and sweat glands; pupillary dilation, ocular accommodation, and heart rate; contraction of the detrusor muscle of the bladder and smooth muscle of the GI tract; and gastric secretion and motility. Doses used to decrease gastric secretions are likely to cause dryness of the mouth (xerostomia) and interfere with visual accommodation, and possibly cause difficulty in urinating.
Various antisecretory effects in the GI tract, including reduction of salivation (producing xerostomia) and gastric secretions (only partial reduction in gastric acid secretion). Prolonged inhibitory effects on the motility of the esophagus, stomach, duodenum, jejunum, ileum, and colon.
Relaxes lower esophageal sphincter with a resultant decrease in lower esophageal sphincter pressure.
Decreases the tone and amplitude of contractions of the ureters and bladder. May cause urinary retention (e.g., in patients with urinary obstruction).
Can reverse reflex vagal cardiac slowing or asystole such as that induced by inhalation of irritant vapors or by vagal stimulation (e.g., carotid sinus stimulation, pressure on the eyeball).
May cause cutaneous vasodilation, especially at toxic doses (atropine flush).
Reduces secretions from the nose, mouth, pharynx, and bronchi. Relaxes smooth muscles of the bronchi and bronchioles with a resultant decrease in airway resistance.
Stimulates the medulla and higher cerebral centers and exhibits CNS effects similar to those produced by antimuscarinics used in the treatment of parkinsonian syndrome (e.g., trihexyphenidyl).
Blocks the responses of the sphincter muscle of the iris and the ciliary muscle of the lens to cholinergic stimulation, producing mydriasis and cycloplegia and a resultant decrease in ocular accommodation. Little effect on IOP except with angle-closure glaucoma where IOP may increase.
Reduces the volume of perspiration by inhibiting sweat-gland secretions. May suppress sweating sufficiently to increase body temperature.
Advice to Patients
Potential for drug to impair mental alertness or physical coordination; avoid driving or operating machinery or performing hazardous work if such effects occur.
Risk of heat prostration, fever, or heat stroke secondary to decreased sweating; caution when febrile, exercising, or when exposed to high environmental temperatures.
Extended-release preparations may not completely disintegrate, and fragments may be excreted in stools.
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
Importance of informing patients of other important precautionary information. (See Cautions.)
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