期刊
AMERICAN JOURNAL OF NEPHROLOGY
卷 32, 期 6, 页码 557-566出版社
KARGER
DOI: 10.1159/000321471
关键词
Salt; Hypertension; Kidney; Oxidative stress; Nitric oxide; beta(1)-Receptor antagonism
资金
- Forest Research Institute
- American Heart Association [2300114]
- NIH [2PO1 HL-051952]
- Farley-Hudson Foundation, Jacksonville, N.C., USA
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL051952] Funding Source: NIH RePORTER
Background: We investigated renal effects of nebivolol, a selective beta(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 reninangiotensin 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 croups. 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. Copyright (E) (C) 2010 S. Karger AG, Basel
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