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Trans. R. Soc. B"],"published-print":{"date-parts":[[2023,6,19]]},"abstract":"<jats:p>\n                    Skeletal and cardiac muscle excitation\u2013contraction coupling commences with Na\n                    <jats:sub>v<\/jats:sub>\n                    1.4\/Na\n                    <jats:sub>v<\/jats:sub>\n                    1.5-mediated, surface and transverse (T-) tubular, action potential generation. This initiates\n                    <jats:italic>feedforward<\/jats:italic>\n                    , allosteric or Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -mediated, T-sarcoplasmic reticular (SR) junctional, voltage sensor-Cav1.1\/Cav1.2 and ryanodine receptor-RyR1\/RyR2 interaction. We review recent structural, physiological and translational studies on possible\n                    <jats:italic>feedback<\/jats:italic>\n                    actions of the resulting SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release on Na\n                    <jats:sub>v<\/jats:sub>\n                    1.4\/Na\n                    <jats:sub>v<\/jats:sub>\n                    1.5 function in native muscle. Finite-element modelling predicted potentially regulatory T-SR junctional [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>TSR<\/jats:sub>\n                    domains. Na\n                    <jats:sub>v<\/jats:sub>\n                    1.4\/Na\n                    <jats:sub>v<\/jats:sub>\n                    1.5, III-IV linker and C-terminal domain structures included Ca\n                    <jats:sup>2+<\/jats:sup>\n                    and\/or calmodulin-binding sites whose mutations corresponded to specific clinical conditions. Loose-patch-clamped native murine skeletal muscle fibres and cardiomyocytes showed reduced Na\n                    <jats:sup>+<\/jats:sup>\n                    currents (\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Na<\/jats:sub>\n                    ) following SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release induced by the Epac and direct RyR1\/RyR2 activators, 8-(4-chlorophenylthio)adenosine-3\u2032,5\u2032-cyclic monophosphate and caffeine, abrogated by the RyR inhibitor dantrolene. Conversely, dantrolene and the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -ATPase inhibitor cyclopiazonic acid increased\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Na<\/jats:sub>\n                    . Experimental, catecholaminergic polymorphic ventricular tachycardic\n                    <jats:italic>RyR2-P2328S<\/jats:italic>\n                    and metabolically deficient\n                    <jats:italic>Pgc1\u03b2<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    cardiomyocytes also showed reduced\n                    <jats:italic>I<\/jats:italic>\n                    <jats:sub>Na<\/jats:sub>\n                    accompanying [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    abnormalities rescued by dantrolene- and flecainide-mediated RyR block. Finally, hydroxychloroquine challenge implicated action potential (AP) prolongation in slowing AP conduction through modifying Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transients. The corresponding tissue\/organ preparations each showed pro-arrhythmic, slowed AP upstrokes and conduction velocities. We finally extend discussion of possible Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -mediated effects to further, Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , K\n                    <jats:sup>+<\/jats:sup>\n                    and Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    , channel types.\n                  <\/jats:p>\n                  <jats:p>This article is part of the theme issue \u2018The heartbeat: its molecular basis and physiological mechanisms\u2019.<\/jats:p>","DOI":"10.1098\/rstb.2022.0162","type":"journal-article","created":{"date-parts":[[2023,5,1]],"date-time":"2023-05-01T02:39:17Z","timestamp":1682908757000},"update-policy":"https:\/\/doi.org\/10.1098\/crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Feedback contributions to excitation\u2013contraction coupling in native functioning striated muscle"],"prefix":"10.1098","volume":"378","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5793-2349","authenticated-orcid":true,"given":"Samantha C.","family":"Salvage","sequence":"first","affiliation":[{"name":"Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9493-4944","authenticated-orcid":true,"given":"Angela F.","family":"Dulhunty","sequence":"additional","affiliation":[{"name":"Eccles Institute of Neuroscience, John Curtin School of Medical Research, The Australian National University, 131 Garran Road, Acton 2601, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamalan","family":"Jeevaratnam","sequence":"additional","affiliation":[{"name":"Faculty of Health and Medical Sciences, University of Surrey, Daphne Jackson Road, Guildford GU2 7XH, 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