Nebivolol Reduces Proteinuria and Renal NADPH Oxidase-Generated Reactive Oxygen Species in the Transgenic Ren2 Rat | Zendy

Adam WhaleyConnell | Zendy; Javad Habibi | Zendy; Megan S. Johnson | Zendy; Roger D. Tilmon | Zendy; Nathan Rehmer | Zendy; Jenna M. Rehmer | Zendy; Charles E. Wiedmeyer | Zendy; Carlos M. Ferrario | Zendy; James R. Sowers | Zendy

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Nebivolol Reduces Proteinuria and Renal NADPH Oxidase-Generated Reactive Oxygen Species in the Transgenic Ren2 Rat

Author(s) -

Adam WhaleyConnell,

Javad Habibi,

Megan S. Johnson,

Roger D. Tilmon,

Nathan Rehmer,

Jenna M. Rehmer,

Charles E. Wiedmeyer,

Carlos M. Ferrario,

James R. Sowers

Publication year - 2009

Publication title -

american journal of nephrology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.394

H-Index - 85

eISSN - 1421-9670

pISSN - 0250-8095

DOI - 10.1159/000229305

Subject(s) - nadph oxidase , nebivolol , apocynin , medicine , endocrinology , reactive oxygen species , nox4 , kidney , nitrotyrosine , proteinuria , angiotensin ii , nitric oxide , oxidative stress , pharmacology , chemistry , nitric oxide synthase , blood pressure , biochemistry

Renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system activation are crucial in the pathogenesis of hypertension, cardiovascular and renal disease. NADPH oxidase-mediated increases in reactive oxygen species (ROS) are an important mediator for RAAS-induced cardiovascular and renal injury. Increased levels of ROS can diminish the bioactivity of nitric oxide (NO), a critical modulator of RAAS effects on the kidney. Thereby, we hypothesized that in vivo nebivolol therapy in a rodent model of activated RAAS would attenuate glomerular damage and proteinuria through its actions to reduce NADPH oxidase activity/ROS and increase bioavailable NO.

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