iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats
It has been suggested that nitric oxide (NO) from iNOS source is involved in inflammation and oxidative stress, and hypertension in obese subjects involves an inflammatory process. However, no study evaluated the participation of iNOS inhibition on cardiovascular, autonomic, and inflammatory paramet...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2017-01-01
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Series: | Clinical and Experimental Hypertension |
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Online Access: | http://dx.doi.org/10.1080/10641963.2016.1210628 |
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author | Natalia Veronez da Cunha Fernanda Novi Cortegoso Lopes Carolina Panis Rubens Cecchini Phileno Pinge-Filho Marli Cardoso Martins-Pinge |
author_facet | Natalia Veronez da Cunha Fernanda Novi Cortegoso Lopes Carolina Panis Rubens Cecchini Phileno Pinge-Filho Marli Cardoso Martins-Pinge |
author_sort | Natalia Veronez da Cunha |
collection | DOAJ |
description | It has been suggested that nitric oxide (NO) from iNOS source is involved in inflammation and oxidative stress, and hypertension in obese subjects involves an inflammatory process. However, no study evaluated the participation of iNOS inhibition on cardiovascular, autonomic, and inflammatory parameters in obese rats. Obesity was induced by the administration of 4 mg/g body weight of monosodium glutamate (MSG) or equimolar saline (CTR) in newborn rats. On the 60th day, treatment with aminoguanidine (Amino, 50 mg/kg), an iNOS inhibitor, or 0.9% saline, was started. On the 90th day, mean arterial pressure (MAP) and heart rate (HR) were recorded in conscious rats and autonomic modulation was conducted with the CardioSeries software. Plasma samples were collected to assess lipid peroxidation and prostaglandins (PGE2). In addition, iNOS immunohistochemistry in cardiac tissue was evaluated. MSG rats showed hypertension compared to CTR, and Amino treatment did not reverse it. Obese rats presented increased sympathetic and decreased parasympathetic modulation to the heart, reverted by Amino treatment. Plasma PGE2 was increased in obese rats, and Amino treatment decreased. Obese rats presented increased plasma lipoperoxidation, which was decreased after Amino treatment. Also, cardiac iNOS immunohistochemistry was decreased after Amino treatment. Our data suggest that iNOS activation is involved in the systemic and cardiac mechanisms of oxidative stress, inflammation, and autonomic dysfunction derived from obesity. |
first_indexed | 2024-03-11T23:46:07Z |
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institution | Directory Open Access Journal |
issn | 1064-1963 1525-6006 |
language | English |
last_indexed | 2024-03-11T23:46:07Z |
publishDate | 2017-01-01 |
publisher | Taylor & Francis Group |
record_format | Article |
series | Clinical and Experimental Hypertension |
spelling | doaj.art-8fd35505d787409fab07c772c5d3ffa12023-09-19T09:24:45ZengTaylor & Francis GroupClinical and Experimental Hypertension1064-19631525-60062017-01-01391505710.1080/10641963.2016.12106281210628iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese ratsNatalia Veronez da Cunha0Fernanda Novi Cortegoso Lopes1Carolina Panis2Rubens Cecchini3Phileno Pinge-Filho4Marli Cardoso Martins-Pinge5State University of LondrinaState University of LondrinaState University of LondrinaState University of LondrinaState University of LondrinaState University of LondrinaIt has been suggested that nitric oxide (NO) from iNOS source is involved in inflammation and oxidative stress, and hypertension in obese subjects involves an inflammatory process. However, no study evaluated the participation of iNOS inhibition on cardiovascular, autonomic, and inflammatory parameters in obese rats. Obesity was induced by the administration of 4 mg/g body weight of monosodium glutamate (MSG) or equimolar saline (CTR) in newborn rats. On the 60th day, treatment with aminoguanidine (Amino, 50 mg/kg), an iNOS inhibitor, or 0.9% saline, was started. On the 90th day, mean arterial pressure (MAP) and heart rate (HR) were recorded in conscious rats and autonomic modulation was conducted with the CardioSeries software. Plasma samples were collected to assess lipid peroxidation and prostaglandins (PGE2). In addition, iNOS immunohistochemistry in cardiac tissue was evaluated. MSG rats showed hypertension compared to CTR, and Amino treatment did not reverse it. Obese rats presented increased sympathetic and decreased parasympathetic modulation to the heart, reverted by Amino treatment. Plasma PGE2 was increased in obese rats, and Amino treatment decreased. Obese rats presented increased plasma lipoperoxidation, which was decreased after Amino treatment. Also, cardiac iNOS immunohistochemistry was decreased after Amino treatment. Our data suggest that iNOS activation is involved in the systemic and cardiac mechanisms of oxidative stress, inflammation, and autonomic dysfunction derived from obesity.http://dx.doi.org/10.1080/10641963.2016.1210628hypertensioninflammationmonosodium glutamatenitric oxideprostaglandinssympathetic |
spellingShingle | Natalia Veronez da Cunha Fernanda Novi Cortegoso Lopes Carolina Panis Rubens Cecchini Phileno Pinge-Filho Marli Cardoso Martins-Pinge iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats Clinical and Experimental Hypertension hypertension inflammation monosodium glutamate nitric oxide prostaglandins sympathetic |
title | iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
title_full | iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
title_fullStr | iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
title_full_unstemmed | iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
title_short | iNOS inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
title_sort | inos inhibition improves autonomic dysfunction and oxidative status in hypertensive obese rats |
topic | hypertension inflammation monosodium glutamate nitric oxide prostaglandins sympathetic |
url | http://dx.doi.org/10.1080/10641963.2016.1210628 |
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