TY - JOUR
T1 - Asenapine modulates nitric oxide release and calcium movements in cardyomyoblasts
AU - ZEPPEGNO, Patrizia
AU - Gramaglia, Carla Maria
AU - Eleonora, GATTONI
AU - Sabrina, GILI
AU - Eleonora, GAMBARO
AU - Elisa, DI TULLIO
AU - Maria Cristina, RIZZA
AU - Serena, FARRUGGIO
AU - Camillo, L.
AU - Mary, D.
AU - Giovanni, VACCA
AU - GROSSINI, Elena
PY - 2016/1/1
Y1 - 2016/1/1
N2 - 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.
AB - 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.
UR - https://iris.uniupo.it/handle/11579/80171
U2 - 10.1016/j.eurpsy.2016.01.2041
DO - 10.1016/j.eurpsy.2016.01.2041
M3 - Article
SN - 0924-9338
VL - 33
SP - S553
JO - European Psychiatry
JF - European Psychiatry
ER -