Nebivolol does not protect against 5/6 ablation/infarction induced chronic kidney disease in rats — Comparison with angiotensin II receptor blockade

摘要: Abstract Aims Nitric oxide (NO) deficiency contributes to chronic kidney disease progression. Nebivolol, a beta adrenergic receptor antagonist, may enhance endogenous NO. Here, we investigated whether Nebivolol attenuates hypertension and renal injury after 5/6 ablation/infarction (A/I). Efficacy was compared the AT1 antagonist Olmesartan. Main methods Kidney were induced by right ablation ~ 2/3 infarction of left kidney. Rats treated orally with vehicle (placebo), (5 mg/kg b.i.d.), or Olmesartan (2.5 mg/kg/day) for 6 weeks A/I. Key findings With placebo, glomerular sclerosis tubulointersititial fibrosis developed increased blood pressure proteinuria, fall in NO x excretion. prevented these changes, but had no effect on measures lowered heart rate. Neither treatment reduced systemic oxidative stress (urinary hydrogen peroxide TBARS). Compared controls, cortex abundance nNOSα decreased nNOSβ rats A/I, changes eNOS. restored nNOSα; however, both nNOSβ. Activity DDAH A/I treatments despite increase protein abundance. manganese SOD fell not Nebivolol. Extracellular copper/zinc abundances changed. Significance In conclusion, showed benefit rapidly progressing, ANG II-dependent model disease. This contrasts protection seen 6 month slowly progressing model.