{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["106(10)"],"submitter":["Jurkat-Rott K"],"pubmed_abstract":["Normal resting potential (P1) of myofibers follows the Nernst equation, exhibiting about -85 mV at a normal extracellular K(+) concentration ([K(+)](o)) of 4 mM. Hyperpolarization occurs with decreased [K(+)](o), although at [K(+)](o) < 1.0 mM, myofibers paradoxically depolarize to a second stable potential of -60 mV (P2). In rat myofiber bundles, P2 also was found at more physiological [K(+)](o) and was associated with inexcitability. To increase the relative frequency of P2 to 50%, [K(+)](o) needed to be lowered to 1.5 mM. In the presence of the ionophore gramicidin, [K(+)](o) reduction to only 2.5 mM yielded the same effect. Acetazolamide normalized this increased frequency of P2 fibers. The findings mimic hypokalemic periodic paralysis (HypoPP), a channelopathy characterized by hypokal"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pagination":["4036-41"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2644652"],"repository":["biostudies-literature"],"pubmed_title":["K+-dependent paradoxical membrane depolarization and Na+ overload, major and reversible contributors to weakness by ion channel leaks."],"pmcid":["PMC2644652"],"pubmed_authors":["Guo XH","Holzherr BD","Jurkat-Rott K","Weber MA","Fauler M","Lehmann-Horn F","Paczulla A","Nordsborg N","Joechle W"],"additional_accession":[]},"is_claimable":false,"name":"K+-dependent paradoxical membrane depolarization and Na+ overload, major and reversible contributors to weakness by ion channel leaks.","description":"Normal resting potential (P1) of myofibers follows the Nernst equation, exhibiting about -85 mV at a normal extracellular K(+) concentration ([K(+)](o)) of 4 mM. Hyperpolarization occurs with decreased [K(+)](o), although at [K(+)](o) < 1.0 mM, myofibers paradoxically depolarize to a second stable potential of -60 mV (P2). In rat myofiber bundles, P2 also was found at more physiological [K(+)](o) and was associated with inexcitability. To increase the relative frequency of P2 to 50%, [K(+)](o) needed to be lowered to 1.5 mM. In the presence of the ionophore gramicidin, [K(+)](o) reduction to only 2.5 mM yielded the same effect. Acetazolamide normalized this increased frequency of P2 fibers. The findings mimic hypokalemic periodic paralysis (HypoPP), a channelopathy characterized by hypokal","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Mar","modification":"2025-05-29T19:44:14.224Z","creation":"2025-05-29T19:44:14.224Z"},"accession":"S-EPMC2644652","cross_references":{"pubmed":["19225109"],"doi":["10.1073/pnas.0811277106"]}}