Editing Suxamethonium chloride (section)

===Phase 1 block===
Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the [[Muscle-type nicotinic receptor|nicotinic acetylcholine]] receptor results in opening of the receptor's [[cation|ion]] channel; a [[depolarization]] of the [[motor end-plate]] occurs and [[calcium]] is released from the [[sarcoplasmic reticulum]] leading to initial muscle contraction and [[fasciculation]]s.<ref name = "Appiah-Ankam_2004">{{cite journal | vauthors = Appiah-Ankam J, Hunter JM | title = Pharmacology of neuromuscular blocking drugs. | journal = Continuing Education in Anaesthesia Critical Care & Pain | date = February 2004 | volume = 4 | issue = 1 | pages = 2–7 | doi = 10.1093/bjaceaccp/mkh002 | doi-access = free }}</ref>

In normal skeletal muscle, [[acetylcholine]] dissociates from the receptor following depolarization and is rapidly hydrolyzed by [[acetylcholinesterase]]. The muscle cell is then ready for the next signal.<ref name = "Appiah-Ankam_2004" />

Suxamethonium is not hydrolyzed by acetylcholinesterase. By remaining bound to the acetylcholine receptor and maintaining the [[membrane potential]] above threshold, it does not allow the muscle cell to completely repolarize. This results in the inability for the voltage gated sodium channels to reset and instead are held in an inactive state leading to an inability to form further action potentials.<ref name = "Appiah-Ankam_2004" />

Voltage gated calcium channels likely close as the partially depolarised membrane potential remains between -30mV and -60mV, which is below the opening of the voltage gated calcium channel, approximately -10mV. Subsequently calcium is removed from the muscle cell [[cytoplasm]] . As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes resulting in muscle [[flaccidity]].<ref>{{cite journal | vauthors = Pelizzari S, Heiss MC, Fernández-Quintero ML, El Ghaleb Y, Liedl KR, Tuluc P, Campiglio M, Flucher BE | title = Ca<sub>V</sub>1.1 voltage-sensing domain III exclusively controls skeletal muscle excitation-contraction coupling | journal = Nature Communications | volume = 15 | issue = 1 | pages = 7440 | date = August 2024 | pmid = 39198449 | doi = 10.1038/s41467-024-51809-5 | pmc = 11358481 }}</ref><ref>{{cite journal | vauthors = Gissen AJ, Nastuk WL | title = Succinylcholine and decamethonium: comparison of depolarization and desensitization | language = en-US | journal = Anesthesiology | volume = 33 | issue = 6 | pages = 611–618 | date = December 1970 | pmid = 5477644 | doi = 10.1097/00000542-197012000-00007 }}</ref>

The results are membrane depolarization and transient fasciculations, followed by flaccid paralysis.