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Inhibition of<jats:styled-content style=\"fixed-case\"><jats:roman>Na<jats:sup>+<\/jats:sup><\/jats:roman><\/jats:styled-content>channels was voltage and<jats:italic>Pertussis<\/jats:italic>toxin (<jats:styled-content style=\"fixed-case\">PTX<\/jats:styled-content>) \u2013 independent. Radioligand\u2010binding studies indicated that specific binding of [<jats:styled-content style=\"fixed-case\"><jats:roman><jats:sup>3<\/jats:sup>H<\/jats:roman><\/jats:styled-content>] batrachotoxin (<jats:styled-content style=\"fixed-case\"><jats:roman>BTX<\/jats:roman><\/jats:styled-content>) to ventricular muscle membranes was also inhibited significantly by 10\u2009\u03bcM met<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>, a non\u2010metabolized<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>analogue, with a marked decrease in B<jats:sub>max<\/jats:sub>values but no change in K<jats:sub>d<\/jats:sub>. Further studies on<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\u2010type<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>channels indicated that<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>potently inhibited these channels (<jats:styled-content style=\"fixed-case\">IC<\/jats:styled-content><jats:sub>50<\/jats:sub>0.1\u2009\u03bcM) in a voltage\u2010 and<jats:styled-content style=\"fixed-case\">PTX<\/jats:styled-content>\u2010independent manner.<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>inhibited maximal amplitudes without affecting the kinetics of<jats:styled-content style=\"fixed-case\"><jats:roman>Ba<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>currents. Met<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>also inhibited<jats:styled-content style=\"fixed-case\"><jats:roman>Na<jats:sup>+<\/jats:sup><\/jats:roman><\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\u2010type<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>currents. Radioligand studies indicated that specific binding of [<jats:styled-content style=\"fixed-case\"><jats:roman><jats:sup>3<\/jats:sup>H<\/jats:roman><\/jats:styled-content>]isradipine, was inhibited significantly by met<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>. (10\u2009\u03bcM), changing B<jats:sub>max<\/jats:sub>but not K<jats:sub>d<\/jats:sub>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and Implications<\/jats:title><jats:p>Results indicate that<jats:styled-content style=\"fixed-case\">AEA<\/jats:styled-content>inhibited the function of voltage\u2010dependent<jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>a<jats:sup>+<\/jats:sup>and<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\u2010type<jats:styled-content style=\"fixed-case\"><jats:roman>Ca<jats:sup>2+<\/jats:sup><\/jats:roman><\/jats:styled-content>channels in rat ventricular myocytes, independent of<jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content><jats:sub>1<\/jats:sub>and<jats:styled-content style=\"fixed-case\">CB<\/jats:styled-content><jats:sub>2<\/jats:sub>receptor 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