The pharmacology of atropine, scopolamine, and glycopyrrolate

Published on 07/02/2015 by admin

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Last modified 07/02/2015

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The pharmacology of atropine, scopolamine, and glycopyrrolate

Niki M. Dietz, MD

Atropine

Atropine is a naturally occurring tertiary amine capable of inhibiting the activation of muscarinic receptors that are found primarily on autonomic effector cells innervated by postganglionic parasympathetic nerves but also present in ganglia and on some cells. At usual doses of the drug, the principal effect of atropine is competitive antagonism of cholinergic stimuli at muscarinic receptors, with little or no effect at nicotinic receptors.

Atropine is derived from flowering plants in the family Solanaceae (e.g., deadly nightshade [Atropa belladonna, named for Atropos, the Fate of Greek mythology who cuts the thread of life], mandrake [Mandragora officinarum], or jimsonweed [Datura stramonium]). Venetian women dropped the juice of deadly nightshade into their eyes to produce mydriasis, which was thought to enhance beauty (hence, the name belladonna, which, translated from Italian, is beautiful woman). Though atropine is used today to treat pesticide poisoning, Solanaceae plants have been used since 200 AD as a biologic weapon to poison, among other substances, wells and wine.

Pharmacokinetics

Absorption

Atropine is well absorbed from the gastrointestinal tract (i.e., from the upper small intestine). It is also well absorbed following intramuscular administration or from the tracheobroncheal tree following inhalation.

Distribution

Atropine undergoes rapid distribution throughout the body, and 50% is plasma protein bound. Atropine crosses the blood-brain barrier and the placenta.

Elimination

The plasma half-life of atropine is 2 to 3 h; it is metabolized in the liver, with 30% to 50% of the drug excreted unchanged in the urine.

Pharmacologic properties

Gastrointestinal system

Atropine reduces the volumes of saliva and gastric secretions. The motility of the entire gastrointestinal tract, from esophagus to colon, is decreased, prolonging transit time. Atropine causes lower esophageal sphincter relaxation through an antimuscarinic mechanism.

Cardiovascular system

The effect of atropine on the heart is dose dependent. An intravenously administered dose of 0.4 to 0.6 mg causes a transient decrease in heart rate of about 8 beats/min, which was once thought to be due to central vagal stimulation but is now known to be mediated through an unknown mechanism. Larger doses of atropine cause progressively increasing tachycardia by blocking vagal effects on M₂ receptors on the sinoatrial node; by the same mechanism, atropine can reverse sinus bradycardia secondary to extracardiac causes but has little or no effect on sinus bradycardia caused by intrinsic disease of the sinoatrial node. Atropine at high doses (>3 mg) may cause cutaneous vasodilation.

Respiratory system

Atropine reduces the volume of secretions from the nose, mouth, pharynx, and bronchi. Along with many other anticholinergic drugs (e.g., ipratropium), it relaxes smooth muscles of bronchi and bronchioles, with resultant decreases in airway resistance.

Central nervous system

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