TNF-α provokes electrical abnormalities in rat atrial myocardium via a NO-dependent mechanism
Stretch-induced depolarizations of cardiomyocytes, which are related to activity of mechano-gated cation channels (MGCs), can lead to serious arrhythmias. However, signaling pathways leading to activation of mechano-gated channels by stretch remain almost unexplored. Using standard sharp microelectr...
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Published in | Pflügers Archiv Vol. 465; no. 12; pp. 1741 - 1752 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Springer Berlin Heidelberg
01.12.2013
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Abstract | Stretch-induced depolarizations of cardiomyocytes, which are related to activity of mechano-gated cation channels (MGCs), can lead to serious arrhythmias. However, signaling pathways leading to activation of mechano-gated channels by stretch remain almost unexplored. Using standard sharp microelectrodes, the present study addresses the hypothesis that tumor necrosis factor-alpha (TNF-α) modulates stretch-induced electrophysiological abnormalities in rat atrial myocardium by a mechanism involving nitric oxide (NO)-dependent pathways. TNF-α (50 ng/ml) produced a marked prolongation of action potential, subsequently transforming into humplike depolarizations and, finally, leading to occurrence of arrhythmias. These effects developed slowly during 25 min of TNF-α application. Similar electrical effects were induced by stretching the preparations. A blocker of MGCs, Gd
3+
(40 μM), completely abolished action potential (AP) prolongations and electrical abnormalities caused by TNF-α or stretch. Further, a donor of exogenous NO,
S
-nitroso-
N
-acetylpenicillamine SNAP (300 μM), evoked the same electrical abnormalities as TNF-α and tissue stretch. Both TNF-α and stretch failed to produce their typical effects after pretreatment of the preparations with the NO-synthase inhibitor L-N
G
-nitroarginine methyl ester (L-NAME) (100 μM). Thus, the present study shows (i) that TNF-α and the NO-donor SNAP evoke MGC-mediated electrical abnormalities in rat atrial myocardium in the absence of stretch that is very similar to stretch-evoked electrical events and (ii) that the TNF-α-induced electrical abnormalities are mediated by NO synthase. In conclusion, our data suggest that NO is an endogenous modulator of MGCs and mediates proarrhythmic effects of TNF-α in mammalian organism. |
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AbstractList | Stretch-induced depolarizations of cardiomyocytes, which are related to activity of mechano-gated cation channels (MGCs), can lead to serious arrhythmias. However, signaling pathways leading to activation of mechano-gated channels by stretch remain almost unexplored. Using standard sharp microelectrodes, the present study addresses the hypothesis that tumor necrosis factor-alpha (TNF-α) modulates stretch-induced electrophysiological abnormalities in rat atrial myocardium by a mechanism involving nitric oxide (NO)-dependent pathways. TNF-α (50 ng/ml) produced a marked prolongation of action potential, subsequently transforming into humplike depolarizations and, finally, leading to occurrence of arrhythmias. These effects developed slowly during 25 min of TNF-α application. Similar electrical effects were induced by stretching the preparations. A blocker of MGCs, Gd
3+
(40 μM), completely abolished action potential (AP) prolongations and electrical abnormalities caused by TNF-α or stretch. Further, a donor of exogenous NO,
S
-nitroso-
N
-acetylpenicillamine SNAP (300 μM), evoked the same electrical abnormalities as TNF-α and tissue stretch. Both TNF-α and stretch failed to produce their typical effects after pretreatment of the preparations with the NO-synthase inhibitor L-N
G
-nitroarginine methyl ester (L-NAME) (100 μM). Thus, the present study shows (i) that TNF-α and the NO-donor SNAP evoke MGC-mediated electrical abnormalities in rat atrial myocardium in the absence of stretch that is very similar to stretch-evoked electrical events and (ii) that the TNF-α-induced electrical abnormalities are mediated by NO synthase. In conclusion, our data suggest that NO is an endogenous modulator of MGCs and mediates proarrhythmic effects of TNF-α in mammalian organism. Stretch-induced depolarizations of cardiomyocytes, which are related to activity of mechano-gated cation channels (MGCs), can lead to serious arrhythmias. However, signaling pathways leading to activation of mechano-gated channels by stretch remain almost unexplored. Using standard sharp microelectrodes, the present study addresses the hypothesis that tumor necrosis factor-alpha (TNF-α) modulates stretch-induced electrophysiological abnormalities in rat atrial myocardium by a mechanism involving nitric oxide (NO)-dependent pathways. TNF-α (50 ng/ml) produced a marked prolongation of action potential, subsequently transforming into humplike depolarizations and, finally, leading to occurrence of arrhythmias. These effects developed slowly during 25 min of TNF-α application. Similar electrical effects were induced by stretching the preparations. A blocker of MGCs, Gd(3+) (40 μM), completely abolished action potential (AP) prolongations and electrical abnormalities caused by TNF-α or stretch. Further, a donor of exogenous NO, S-nitroso-N-acetylpenicillamine SNAP (300 μM), evoked the same electrical abnormalities as TNF-α and tissue stretch. Both TNF-α and stretch failed to produce their typical effects after pretreatment of the preparations with the NO-synthase inhibitor L-N(G)-nitroarginine methyl ester (L-NAME) (100 μM). Thus, the present study shows (i) that TNF-α and the NO-donor SNAP evoke MGC-mediated electrical abnormalities in rat atrial myocardium in the absence of stretch that is very similar to stretch-evoked electrical events and (ii) that the TNF-α-induced electrical abnormalities are mediated by NO synthase. In conclusion, our data suggest that NO is an endogenous modulator of MGCs and mediates proarrhythmic effects of TNF-α in mammalian organism. |
Author | Kamkin, Andre Mitrochin, Vadim M. Schubert, Rudolf Kuzmin, Vladislav S. Kalugin, Leonid Dvorzhak, Anton Makarenko, Ekaterina Y. Abramochkin, Denis V. |
Author_xml | – sequence: 1 givenname: Denis V. surname: Abramochkin fullname: Abramochkin, Denis V. email: abram340@mail.ru organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University, Department of Human and Animal Physiology, Moscow State University, Lomonosov Moscow State University – sequence: 2 givenname: Vladislav S. surname: Kuzmin fullname: Kuzmin, Vladislav S. organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University, Department of Human and Animal Physiology, Moscow State University – sequence: 3 givenname: Vadim M. surname: Mitrochin fullname: Mitrochin, Vadim M. organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University – sequence: 4 givenname: Leonid surname: Kalugin fullname: Kalugin, Leonid organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University – sequence: 5 givenname: Anton surname: Dvorzhak fullname: Dvorzhak, Anton organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University, Synaptic Dysfunction Group, Exzellenzcluster Neurocure, Abt. Exp. Neurologie, Charité–Universitätsmedizin – sequence: 6 givenname: Ekaterina Y. surname: Makarenko fullname: Makarenko, Ekaterina Y. organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University – sequence: 7 givenname: Rudolf surname: Schubert fullname: Schubert, Rudolf organization: Centre for Biomedicine and Medical Technology Mannheim (CBTM), Research Division Cardiovascular Physiology, Medical Faculty Mannheim, Heidelberg University – sequence: 8 givenname: Andre surname: Kamkin fullname: Kamkin, Andre organization: Department of Fundamental and Applied Physiology, Russian National Research Medical University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23827962$$D View this record in MEDLINE/PubMed |
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Keywords | Heart Stretch Atrium NO Action potential Cytokine |
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Snippet | Stretch-induced depolarizations of cardiomyocytes, which are related to activity of mechano-gated cation channels (MGCs), can lead to serious arrhythmias.... |
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SubjectTerms | Action Potentials - drug effects Animals Arrhythmias, Cardiac - chemically induced Atrial Function - drug effects Atrial Function - physiology Biomedical and Life Sciences Biomedicine Cell Biology Electrophysiology Gadolinium - pharmacology Heart Atria - metabolism Human Physiology Ion Channels Male Membrane Potentials - drug effects Molecular Medicine Myocytes, Cardiac - drug effects Myocytes, Cardiac - physiology Neurosciences Nitric Oxide - physiology Physical Stimulation Rats Rats, Wistar Receptors Receptors and Transporters S-Nitroso-N-Acetylpenicillamine - pharmacology Tumor Necrosis Factor-alpha - pharmacology |
Title | TNF-α provokes electrical abnormalities in rat atrial myocardium via a NO-dependent mechanism |
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