Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension
Oxidative stress produced through reactive oxygen species (ROS) enhancement is considered to play a key role in the development and maintenance of hypertension. In the vasculature, the most important source of ROS is the reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase enzyme. T...
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2009
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01602446_v54_n4_p348_Polizio http://hdl.handle.net/20.500.12110/paper_01602446_v54_n4_p348_Polizio |
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paper:paper_01602446_v54_n4_p348_Polizio2023-06-08T15:13:24Z Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension Angiotensin II Antihypertensive drugs Aorta Arterial pressure Oxidative stress angiotensin II heme oxygenase 1 losartan minoxidil reactive oxygen metabolite reduced nicotinamide adenine dinucleotide phosphate oxidase superoxide animal experiment animal model animal tissue arterial pressure article controlled study enzyme activity hypertension male nitrosative stress nonhuman oxidative stress priority journal protein expression rat thoracic aorta Animals Antihypertensive Agents Aorta, Thoracic Blood Pressure Disease Models, Animal Heme Oxygenase (Decyclizing) Hypertension, Renal Losartan Male Minoxidil NADPH Oxidase Oxidative Stress Rats Rats, Wistar Reactive Oxygen Species Oxidative stress produced through reactive oxygen species (ROS) enhancement is considered to play a key role in the development and maintenance of hypertension. In the vasculature, the most important source of ROS is the reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase enzyme. The principal stimulus of this enzyme is angiotensin II (Ang II). However, oxidative stress seems to be present in virtually all forms of hypertension including low-renin hypertension, where the levels of Ang II are reduced. For this reason, the question is if ROS generation is induced by Ang II or it is a consequence of hypertension. We used as hypertensive model the aortic coarctated rats, which were treated with losartan or minoxidil for 7 days. Thoracic aortic segments were excised, and the NAD(P)H oxidase subunits expression, oxidative stress parameters, and heme oxygenase-1 abundance were evaluated. Hypertensive animals had an increase in the activity and expression of NAD(P)H oxidase and, as a consequence, in the oxidative stress parameters. Interestingly, either losartan or minoxidil administration blunted those parameters, indicating that arterial pressure is the key factor in the development of oxidative stress in the hypertensive aorta. We suggest that antihypertensive drug administration at the beginning of this pathology delays the oxidative stress generation, thus preventing the aggravation of this disease. Copyright © 2009 by Lippincott Williams & Wilkins. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01602446_v54_n4_p348_Polizio http://hdl.handle.net/20.500.12110/paper_01602446_v54_n4_p348_Polizio |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Angiotensin II Antihypertensive drugs Aorta Arterial pressure Oxidative stress angiotensin II heme oxygenase 1 losartan minoxidil reactive oxygen metabolite reduced nicotinamide adenine dinucleotide phosphate oxidase superoxide animal experiment animal model animal tissue arterial pressure article controlled study enzyme activity hypertension male nitrosative stress nonhuman oxidative stress priority journal protein expression rat thoracic aorta Animals Antihypertensive Agents Aorta, Thoracic Blood Pressure Disease Models, Animal Heme Oxygenase (Decyclizing) Hypertension, Renal Losartan Male Minoxidil NADPH Oxidase Oxidative Stress Rats Rats, Wistar Reactive Oxygen Species |
| spellingShingle |
Angiotensin II Antihypertensive drugs Aorta Arterial pressure Oxidative stress angiotensin II heme oxygenase 1 losartan minoxidil reactive oxygen metabolite reduced nicotinamide adenine dinucleotide phosphate oxidase superoxide animal experiment animal model animal tissue arterial pressure article controlled study enzyme activity hypertension male nitrosative stress nonhuman oxidative stress priority journal protein expression rat thoracic aorta Animals Antihypertensive Agents Aorta, Thoracic Blood Pressure Disease Models, Animal Heme Oxygenase (Decyclizing) Hypertension, Renal Losartan Male Minoxidil NADPH Oxidase Oxidative Stress Rats Rats, Wistar Reactive Oxygen Species Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| topic_facet |
Angiotensin II Antihypertensive drugs Aorta Arterial pressure Oxidative stress angiotensin II heme oxygenase 1 losartan minoxidil reactive oxygen metabolite reduced nicotinamide adenine dinucleotide phosphate oxidase superoxide animal experiment animal model animal tissue arterial pressure article controlled study enzyme activity hypertension male nitrosative stress nonhuman oxidative stress priority journal protein expression rat thoracic aorta Animals Antihypertensive Agents Aorta, Thoracic Blood Pressure Disease Models, Animal Heme Oxygenase (Decyclizing) Hypertension, Renal Losartan Male Minoxidil NADPH Oxidase Oxidative Stress Rats Rats, Wistar Reactive Oxygen Species |
| description |
Oxidative stress produced through reactive oxygen species (ROS) enhancement is considered to play a key role in the development and maintenance of hypertension. In the vasculature, the most important source of ROS is the reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase enzyme. The principal stimulus of this enzyme is angiotensin II (Ang II). However, oxidative stress seems to be present in virtually all forms of hypertension including low-renin hypertension, where the levels of Ang II are reduced. For this reason, the question is if ROS generation is induced by Ang II or it is a consequence of hypertension. We used as hypertensive model the aortic coarctated rats, which were treated with losartan or minoxidil for 7 days. Thoracic aortic segments were excised, and the NAD(P)H oxidase subunits expression, oxidative stress parameters, and heme oxygenase-1 abundance were evaluated. Hypertensive animals had an increase in the activity and expression of NAD(P)H oxidase and, as a consequence, in the oxidative stress parameters. Interestingly, either losartan or minoxidil administration blunted those parameters, indicating that arterial pressure is the key factor in the development of oxidative stress in the hypertensive aorta. We suggest that antihypertensive drug administration at the beginning of this pathology delays the oxidative stress generation, thus preventing the aggravation of this disease. Copyright © 2009 by Lippincott Williams & Wilkins. |
| title |
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| title_short |
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| title_full |
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| title_fullStr |
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| title_full_unstemmed |
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| title_sort |
lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hypertension |
| publishDate |
2009 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01602446_v54_n4_p348_Polizio http://hdl.handle.net/20.500.12110/paper_01602446_v54_n4_p348_Polizio |
| _version_ |
1768543272652767232 |