Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effectsin vivoin a mouse model of hypertrophic cardiomyopathy | Zendy

Frederik Flenner | Zendy; Felix W. Friedrich | Zendy; Nele Ungeheuer | Zendy; Torsten Christ | Zendy; Birgit Geertz | Zendy; Silke Reischmann | Zendy; Stefan Wagner | Zendy; Κωνσταντίνα Σταθοπούλου | Zendy; KlausDieter Söhren | Zendy; Florian Weinberger | Zendy; Edzard Schwedhelm | Zendy; Friederike Cuello | Zendy; Lars S. Maier | Zendy; Thomas Eschenhagen | Zendy; Lucie Carrier | Zendy

Open Access

Ranolazine antagonizes catecholamine-induced dysfunction in isolated cardiomyocytes, but lacks long-term therapeutic effectsin vivoin a mouse model of hypertrophic cardiomyopathy

Author(s) -

Frederik Flenner,

Felix W. Friedrich,

Nele Ungeheuer,

Torsten Christ,

Birgit Geertz,

Silke Reischmann,

Stefan Wagner,

Κωνσταντίνα Σταθοπούλου,

KlausDieter Söhren,

Florian Weinberger,

Edzard Schwedhelm,

Friederike Cuello,

Lars S. Maier,

Thomas Eschenhagen,

Lucie Carrier

Publication year - 2015

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvv247

Subject(s) - ranolazine , myofilament , medicine , sarcomere , lusitropy , diastole , myocyte , endocrinology , hypertrophic cardiomyopathy , cardiology , prazosin , chemistry , blood pressure , receptor , antagonist

Hypertrophic cardiomyopathy (HCM) is often accompanied by increased myofilament Ca(2+) sensitivity and diastolic dysfunction. Recent findings indicate increased late Na(+) current density in human HCM cardiomyocytes. Since ranolazine has the potential to decrease myofilament Ca(2+) sensitivity and late Na(+) current, we investigated its effects in an Mybpc3-targeted knock-in (KI) mouse model of HCM.

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