Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/55179
Title: Acetylcholine Attenuates Hydrogen Peroxide-Induced Intracellular Calcium Dyshomeostasis Through Both Muscarinic and Nicotinic Receptors in Cardiomyocytes
Authors: Siripong Palee
Nattayaporn Apaijai
Krekwit Shinlapawittayatorn
Siriporn C. Chattipakorn
Nipon Chattipakorn
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Jul-2016
Abstract: © 2016 The Author(s) Published by S. Karger AG, Basel. Background/Aims: Oxidative stress induced intracellular Ca2+overload plays an important role in the pathophysiology of several heart diseases. Acetylcholine (ACh) has been shown to suppress reactive oxygen species generation during oxidative stress. However, there is little information regarding the effects of ACh on the intracellular Ca2+regulation in the presence of oxidative stress. Therefore, we investigated the effects of ACh applied before or after hydrogen peroxide (H2O2) treatment on the intracellular Ca2+regulation in isolated cardiomyocytes. Methods: Single ventricular myocytes were isolated from the male Wistar rats for the intracellular Ca2+transient study by a fluorimetric ratio technique. Results: H2O2significantly decreased both of intracellular Ca2+transient amplitude and decay rate. ACh applied before, but not after, H2O2treatment attenuated the reduction of intracellular Ca2+transient amplitude and decay rate. Both atropine (a muscarinic acetylcholine receptor blocker) and mecamylamine (a nicotinic acetylcholine receptor blocker) significantly decreased the protective effects of acetylcholine on the intracellular Ca2+regulation. Moreover, the combination of atropine and mecamylamine completely abolished the protective effects of acetylcholine on intracellular Ca2+transient amplitude and decay rate. Conclusion: ACh pretreatment attenuates H2O2-induced intracellular Ca2+dyshomeostasis through both muscarinic and nicotinic receptors.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84976586868&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/55179
ISSN: 14219778
10158987
Appears in Collections:CMUL: Journal Articles

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