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Asenapine modulates nitric oxide release and calcium movements in cardyomyoblasts

Published online by Cambridge University Press:  23 March 2020

P. Zeppegno ,
C. Gramaglia ,
E. Gattoni ,
S. Gili ,
E. Gambaro ,
E. Di Tullio ,
M.C. Rizza ,
S. Farruggio ,
L. Camillo  and
D. Mary
...Show all authors
C. Gramaglia
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
E. Gattoni
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
S. Gili
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
E. Gambaro
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
E. Di Tullio
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
M.C. Rizza
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
S. Farruggio
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
L. Camillo
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
D. Mary
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
G. Vacca
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy
E. Grossini
Affiliation:
University of Eastern Piedmont, Traslational Medicine, Novara, Italy

Abstract

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Objective

To examine the effects of asenapine on NO release and Ca2+ transients in H9C2, which were either subjected to peroxidation or not.

Materials and methods

H9C2 were treated with asenapine alone or in presence of intracellular kinases 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 the 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.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
EV1056
Information
European Psychiatry , Volume 33 , Issue S1: Abstracts of the 24th European Congress of Psychiatry , March 2016 , pp. S553
Copyright
Copyright © European Psychiatric Association 2016
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