CIPYP   05508
CENTRO DE INVESTIGACIONES SOBRE PORFIRINAS Y PORFIRIAS
Unidad Ejecutora - UE
artículos
Título:
Lowering arterial pressure delays the oxidative stress generation in a renal experimental model of hipertensión
Autor/es:
POLIZIO, ARIEL H.; GORZALCZANY, SUSANA; TOMARO, MARÍA L.
Revista:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Editorial:
Springer
Referencias:
Lugar: Amsterdam; Año: 2009 vol. 54 p. 348 - 354
ISSN:
0160-2446
Resumen:
Abstract: 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.
(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.
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.