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    Journal of Pharmacology and PharmacotherapeuticsNOW IN
    Article

    Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

    Elena Grossini2,3★, Carla Gramaglia3,4, Serena Farruggio2,3, Lara Camillo3,4, David Mary2,3, Giovanni Vacca2,3, Patrizia Zeppegno3,4★ Corresponding author

    1. 1Department of Translational Medicine, Laboratory of Physiology and Experimental Surgery, University of Eastern Piedmont “A. Avogadro”, Italy.
    2. 2Azienda Ospedaliera Universitaria Maggiore Della Carità, Corso Mazzini 36, Novara, Italy.
    3. 3Department of Translational Medicine, Psichiatric Unit, University of Eastern Piedmont “A. Avogadro”, Via Solaroli 17, I‑28100, Italy.

    CORRESPONDENCE

    Elena Grossini

    Azienda Ospedaliera Universitaria Maggiore Della Carità, Corso Mazzini 36, Novara, Italy.

    elena.grossini@med.uniupo.it

    Received: 28-09-2015; Revised: 09-11-2015; Accepted: 01-02-2016.

    Volume 7, Issue 1 · pp. 6–14 · PUBLISHED 2016 · DOI: 10.4103/0976-500X.179358

    View on J Pharmacol. Pharmacother. original site ↗

    ABSTRACT

    Objective: To examine the effects of asenapine on nitric oxide (NO) release and Ca2+ transients in H9C2 cell line, which were either subjected to peroxidation or not. Materials and Methods: H9C2 were treated with asenapine alone or in presence of intracellular kinase blockers, serotoninergic and dopaminergic antagonists, and voltage Ca2+ channels inhibitors. Experiments were also performed in H9C2 treated with hydrogen peroxide. NO release and intracellular Ca2+ were measured through specific probes. Results: In H9C2, asenapine differently modulated NO release and Ca2+ movements depending on peroxidative condition. The Ca2+ pool mobilized by asenapine mainly originated from the extracellular space and was slightly affected by thapsigargin. Moreover, the effects of asenapine were reduced or prevented by kinases blockers, dopaminergic and serotoninergic receptors inhibitors, and voltage Ca2+ channels blockers. Conclusions: On the basis of our findings, we can conclude that asenapine by interacting with its specific receptors, exerts dual effects on NO release and Ca2+ homeostasis in H9C2; this would be of particular clinical relevance when considering their role in cardiac function modulation.

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      Grossini, E., Gramaglia, C., Farruggio, S., Camillo, L., Mary, D., Vacca, G., & Zeppegno, P. (2016). Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts. Journal of Pharmacology and Pharmacotherapeutics, 7(1), 6–14. https://doi.org/10.4103/0976-500X.179358