ArticleJournal of pharmacology & pharmacotherapeutics
Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts.
Article in Journal of pharmacology & pharmacotherapeutics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Call to action regarding the vascular-bipolar link: A report from the Vascular Task Force of the International Society for Bipolar Disorders.Bipolar disorders · 2020Review
- Preeclampsia and intrauterine growth restriction: Role of human umbilical cord mesenchymal stem cells-trophoblast cross-talk.PloS one · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo examine the effects of asenapine on nitric oxide (NO) release and Ca(2+) transients in H9C2 cell line, which were either subjected to peroxidation or not. MATERIALS AND
methodsH9C2 were treated with asenapine alone or in presence of intracellular kinase blockers, serotoninergic and dopaminergic antagonists, and voltage Ca(2+) channels inhibitors. Experiments were also performed in H9C2 treated with hydrogen peroxide. NO release and intracellular Ca(2+) were measured through specific probes.
resultsIn H9C2, asenapine differently modulated NO release and Ca(2+) movements depending on peroxidative condition. The Ca(2+) 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 Ca(2+) channels blockers.
conclusionsOn the basis of our findings, we can conclude that asenapine by interacting with its specific receptors, exerts dual effects on NO release and Ca(2+) homeostasis in H9C2; this would be of particular clinical relevance when considering their role in cardiac function modulation.
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