{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kanaporis G"],"funding":["NHLBI NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["51-67"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9878619"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["601(1)"],"pubmed_abstract":["At the cellular level, cardiac alternans is observed as beat-to-beat alternations in contraction strength, action potential (AP) morphology and Ca<sup>2+</sup> transient (CaT) amplitude, and is a risk factor for cardiac arrhythmia. The (patho)physiological roles of small conductance Ca<sup>2+</sup> -activated K<sup>+</sup> (SK) channels in ventricles are poorly understood. We tested the hypothesis that in single rabbit ventricular myocytes pharmacological modulation of SK channels plays a causative role for the development of pacing-induced CaT and AP duration (APD) alternans. SK channel blockers (apamin, UCL1684) had only a minor effect on AP repolarization. However, SK channel activation by NS309 resulted in significant APD shortening, demonstrating that functional SK channels are well e"],"journal":["The Journal of physiology"],"pubmed_title":["Activation of small conductance Ca<sup>2+</sup> -activated K<sup>+</sup> channels suppresses Ca<sup>2+</sup> transient and action potential alternans in ventricular myocytes."],"pmcid":["PMC9878619"],"funding_grant_id":["HL134781","HL057832","R01 HL132871","R01 HL057832","R01 HL164453","HL132871","R01 HL155762","R01 HL134781","HL155762","HL164453"],"pubmed_authors":["Kanaporis G","Blatter LA"],"additional_accession":[]},"is_claimable":false,"name":"Activation of small conductance Ca<sup>2+</sup> -activated K<sup>+</sup> channels suppresses Ca<sup>2+</sup> transient and action potential alternans in ventricular myocytes.","description":"At the cellular level, cardiac alternans is observed as beat-to-beat alternations in contraction strength, action potential (AP) morphology and Ca<sup>2+</sup> transient (CaT) amplitude, and is a risk factor for cardiac arrhythmia. The (patho)physiological roles of small conductance Ca<sup>2+</sup> -activated K<sup>+</sup> (SK) channels in ventricles are poorly understood. We tested the hypothesis that in single rabbit ventricular myocytes pharmacological modulation of SK channels plays a causative role for the development of pacing-induced CaT and AP duration (APD) alternans. SK channel blockers (apamin, UCL1684) had only a minor effect on AP repolarization. However, SK channel activation by NS309 resulted in significant APD shortening, demonstrating that functional SK channels are well e","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-26T07:48:10.035Z","creation":"2025-04-06T12:29:44.846Z"},"accession":"S-EPMC9878619","cross_references":{"pubmed":["36426548"],"doi":["10.1113/jp283870","10.1113/JP283870"]}}