IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
artículos
Título:
Losartan exerts renoprotection through NAD(P)H oxidase downregulation in a renovascular model of hypertension
Autor/es:
ARIEL H. POLIZIO; KARINA B. BALESTRASSE; GERMAN G. GORNALUSSE; SUSANA B. GORZALCZANY; DIEGO M. SANTA CRUZ; GUSTAVO G. YANNARELLI; CLARA PEÑA; MARIA L. TOMARO
Revista:
REGULATORY PEPTIDES
Editorial:
ELSEVIER SCIENCE BV
Referencias:
Año: 2009 vol. 156 p. 28 - 33
ISSN:
0167-0115
Resumen:
a b s t r a c t
Article history:
Received 31 July 2008
Received in revised form 1 April 2009
Accepted 6 May 2009
Available online xxxx
Keywords:
Angiotensin II
Antioxidant enzymes
Arterial pressure
Kidney
Oxidative stress
Aortic coarctation
This study was performed to provide insight into the regulatory role of angiotensin II and arterial pressure on
the activity of antioxidant enzymes and oxidative stress generation in the hypertensive kidney from an
experimental animal model of renovascular hypertension. Aortic coarcted and sham-operated rats received
vehicle, losartan or minoxidil in their drinking water. After 7 d of treatment rats were sacrificed; hypertensive
kidneys were excised, and the NAD(P)H oxidase subunits expression, TBARS production, glutathione level
and the activity of heme oxygenase-1 and classical antioxidant enzymes, were evaluated. Losartan
administration significantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
kidneys were excised, and the NAD(P)H oxidase subunits expression, TBARS production, glutathione level
and the activity of heme oxygenase-1 and classical antioxidant enzymes, were evaluated. Losartan
administration significantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
kidneys were excised, and the NAD(P)H oxidase subunits expression, TBARS production, glutathione level
and the activity of heme oxygenase-1 and classical antioxidant enzymes, were evaluated. Losartan
administration significantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
kidneys were excised, and the NAD(P)H oxidase subunits expression, TBARS production, glutathione level
and the activity of heme oxygenase-1 and classical antioxidant enzymes, were evaluated. Losartan
administration significantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
ficed; hypertensive
kidneys were excised, and the NAD(P)H oxidase subunits expression, TBARS production, glutathione level
and the activity of heme oxygenase-1 and classical antioxidant enzymes, were evaluated. Losartan
administration significantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.
ficantly reduced oxidative stress generation decreasing NAD(P)H oxidase expression,
independently of the drop in arterial pressure. On the other hand, antioxidant enzymes were regulated by
arterial pressure and they were not implicated in kidney protection against oxidative damage. Findings here
reported strongly suggest that clinical therapeutics with the Ang II type 1 receptor blocker prevents oxidative
stress generation and may attenuate the kidney oxidative damage in the renovascular hypertension. We
hypothesize that the pathway followed by the Ang II blocker to achieve this renoprotection, though
independent of the primary antioxidant enzymatic system, depends on NAD(P)H oxidase downregulation.
© 2009 Elsevier B.V. All rights reserved.