Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions
Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two grou...
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| Format: | Article |
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MDPI AG
2019-04-01
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| Series: | Molecules |
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| Online Access: | https://www.mdpi.com/1420-3049/24/9/1682 |
| _version_ | 1819173441100578816 |
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| author | Michaela Kosutova Olga Pechanova Andrej Barta Sona Franova Martina Cebova |
| author_facet | Michaela Kosutova Olga Pechanova Andrej Barta Sona Franova Martina Cebova |
| author_sort | Michaela Kosutova |
| collection | DOAJ |
| description | Myocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes. |
| first_indexed | 2024-12-22T20:23:07Z |
| format | Article |
| id | doaj.art-61078eede290460aa281fec548ac5525 |
| institution | Directory Open Access Journal |
| issn | 1420-3049 |
| language | English |
| last_indexed | 2024-12-22T20:23:07Z |
| publishDate | 2019-04-01 |
| publisher | MDPI AG |
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| series | Molecules |
| spelling | doaj.art-61078eede290460aa281fec548ac55252022-12-21T18:13:47ZengMDPI AGMolecules1420-30492019-04-01249168210.3390/molecules24091682molecules24091682Different adaptive NO-dependent Mechanisms in Normal and Hypertensive ConditionsMichaela Kosutova0Olga Pechanova1Andrej Barta2Sona Franova3Martina Cebova4Institute of Normal and Pathological Physiology, Centre of Experimental Medicine SAS, Sienkiewiczova 1, 813 71 Bratislava, Slovak RepublicInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine SAS, Sienkiewiczova 1, 813 71 Bratislava, Slovak RepublicInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine SAS, Sienkiewiczova 1, 813 71 Bratislava, Slovak RepublicDepartment of Pharmacology, Biomedical Centre JFM CU, Comenius University Bratislava, Jessenius Faculty of Medicine Martin, Malá Hora, 11161/4C, 036 01 Martin, Slovak RepublicInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine SAS, Sienkiewiczova 1, 813 71 Bratislava, Slovak RepublicMyocardial infarction (MI) remains the leading cause of death worldwide. We aimed to investigate the effect of NO deficiency on selective biochemical parameters within discreet myocardial zones after experimentally induced MI. To induce MI, the left descending coronary artery was ligated in two groups of 16-week-old WKY rats. In one group, NO production was inhibited by L-NAME (20 mg/kg/day) administration four weeks prior to ligation. Sham operations were performed on both groups as a control. Seven days after MI, we evaluated levels of nitric oxide synthase (NOS) activity, eNOS, iNOS, NFҡB/p65 and Nrf2 in ischemic, injured and non-ischemic zones of the heart. Levels of circulating TNF-α and IL-6 were evaluated in the plasma. MI led to increased NOS activity in all investigated zones of myocardium as well as circulating levels of TNF-α and IL-6. L-NAME treatment decreased NOS activity in the heart of sham operated animals. eNOS expression was increased in the injured zone and this could be a compensatory mechanism that improves the perfusion of the myocardium and cardiac dysfunction. Conversely, iNOS expression increased in the infarcted zone and may contribute to the inflammatory process and irreversible necrotic changes.https://www.mdpi.com/1420-3049/24/9/1682myocardial infarctionL-NAMEnitric oxide |
| spellingShingle | Michaela Kosutova Olga Pechanova Andrej Barta Sona Franova Martina Cebova Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions Molecules myocardial infarction L-NAME nitric oxide |
| title | Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions |
| title_full | Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions |
| title_fullStr | Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions |
| title_full_unstemmed | Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions |
| title_short | Different adaptive NO-dependent Mechanisms in Normal and Hypertensive Conditions |
| title_sort | different adaptive no dependent mechanisms in normal and hypertensive conditions |
| topic | myocardial infarction L-NAME nitric oxide |
| url | https://www.mdpi.com/1420-3049/24/9/1682 |
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