Editing Atropine (section)

==Pharmacology==
{{More medical citations needed|date=January 2022}}
In general, atropine counters the "rest and digest" activity of [[gland]]s regulated by the [[parasympathetic nervous system]], producing clinical effects such as increased heart rate and delayed gastric emptying. This occurs because atropine is a competitive, reversible antagonist of the [[muscarinic acetylcholine receptor]]s ([[acetylcholine]] being the main [[neurotransmitter]] used by the parasympathetic nervous system).

Atropine is a [[competitive antagonist]] of the [[muscarinic acetylcholine receptor]] types [[Muscarinic acetylcholine receptor M1|M1]], [[Muscarinic acetylcholine receptor M2|M2]], [[Muscarinic acetylcholine receptor M3|M3]], [[Muscarinic acetylcholine receptor M4|M4]] and [[Muscarinic acetylcholine receptor M5|M5]].<ref>{{cite book | vauthors = Rang HP, Dale MM, Ritter JM, Moore P |title=Pharmacology |page=139 |publisher=Elsevier |year=2003 | isbn = 978-0-443-07145-4 }}</ref> It is classified as an [[anticholinergic drug]] ([[parasympatholytic]]).

In cardiac uses, it works as a nonselective muscarinic acetylcholinergic antagonist, increasing firing of the [[sinoatrial node]] (SA) and conduction through the [[atrioventricular node]] (AV) of the [[heart]], opposes the actions of the [[vagus nerve]], blocks [[acetylcholine]] [[receptor (biochemistry)|receptor]] sites, and decreases [[bronchial]] [[secretion]]s.

In the eye, atropine induces [[mydriasis]] by blocking the contraction of the circular [[pupillary sphincter]] muscle, which is normally stimulated by acetylcholine release, thereby allowing the radial [[iris dilator muscle]] to contract and dilate the [[pupil]]. Atropine induces [[cycloplegia]] by paralyzing the [[ciliary muscle]]s, whose action inhibits accommodation to allow accurate refraction in children, helps to relieve pain associated with [[iridocyclitis]], and treats ciliary block (malignant) [[glaucoma]].

The vagus (parasympathetic) nerves that innervate the heart release acetylcholine (ACh) as their primary neurotransmitter. ACh binds to muscarinic receptors (M2) that are found principally on cells comprising the sinoatrial (SA) and atrioventricular (AV) nodes. Muscarinic receptors are coupled to the [[Gi alpha subunit|G<sub>i</sub> subunit]]; therefore, vagal activation decreases cAMP. Gi-protein activation also leads to the activation of [[KACh channel]]s that increase potassium efflux and hyperpolarizes the cells.

Increases in vagal activities to the SA node decrease the firing rate of the pacemaker cells by decreasing the slope of the pacemaker potential (phase 4 of the action potential); this decreases heart rate (negative chronotropy). The change in phase 4 slope results from alterations in potassium and calcium currents, as well as the slow-inward sodium current that is thought to be responsible for the pacemaker current (If). By hyperpolarizing the cells, vagal activation increases the cell's threshold for firing, which contributes to the reduction in the firing rate. Similar electrophysiological effects also occur at the AV node; however, in this tissue, these changes are manifested as a reduction in impulse conduction velocity through the AV node (negative dromotropy). In the resting state, there is a large degree of vagal tone in the heart, which is responsible for low resting heart rates.

There is also some vagal innervation of the atrial muscle, and to a much lesser extent, the ventricular muscle. Vagus activation, therefore, results in modest reductions in atrial contractility (inotropy) and even smaller decreases in ventricular contractility.

Muscarinic receptor antagonists bind to muscarinic receptors thereby preventing ACh from binding to and activating the receptor. By blocking the actions of ACh, muscarinic receptor antagonists very effectively block the effects of vagal nerve activity on the heart. By doing so, they increase heart rate and conduction velocity.