Salt-induced renal injury in spontaneously hypertensive rats: effects of nebivolol.
Am J Nephrol
; 32(6): 557-66, 2010.
Article
em En
| MEDLINE
| ID: mdl-21042014
ABSTRACT
BACKGROUND:
we investigated renal effects of nebivolol, a selective ß(1)-receptor blocker with additional antioxidative ability, in spontaneously hypertensive rats (SHR) where increased salt intake induces oxidative stress and worsens renal function as a result of further activation of the renin-angiotensin and sympathetic nervous systems.METHODS:
male SHR were given an 8% salt diet (HS; n = 22) for 5 weeks; their age-matched controls (n = 9) received standard chow. Nebivolol was given at a dose of 10 mg/kg/day for 5 weeks in 11 HS rats.RESULTS:
HS increased blood pressure, plasma renin concentration, urinary protein excretion, and renal nitroxidative stress while decreasing renal blood flow and angiotensin 1-7 receptor (mas) protein expression. There was no change in angiotensin II type 1 receptor expression among the experimental groups. Nebivolol did not alter the salt-induced increase in blood pressure but reduced urinary protein excretion, plasma renin concentration, and nitroxidative stress. Nebivolol also increased neuronal NOS expression while preventing the salt-induced decrease in renal blood flow and mas protein expression.CONCLUSION:
nebivolol prevented salt-induced kidney injury and associated proteinuria in SHR through a blood pressure-independent mechanism. Its protective effects may be related to reduction in oxidative stress, increases in neuronal NOS and restoration of angiotensin II type 1/mas receptor balance.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Sistema Renina-Angiotensina
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Benzopiranos
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Cloreto de Sódio
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Etanolaminas
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Antagonistas de Receptores Adrenérgicos beta 1
Limite:
Animals
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article