Asenapine modulates nitric oxide release and calcium movements in cardyomyoblasts

Abstract

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.