Nipradilol prevents L-NAME-exacerbated nephrosclerosis with decreasing of caspase-3 expression in SHR.

摘要: The proliferative cell nuclear antigen (PCNA) is an auxiliary protein of DNA polymerase δand appears to be required for both synthesis and repair. Previously, we showed that prolonged NO synthase (NOS) inhibition produced severe nephrosclerosis with increase glomerular fragmentation (apoptosis), ischemia hypertension in spontaneously hypertensive rats (SHR). objective the present study was investigate effects vasodilating, nonselective, NO-releasing β-adrenoceptor blocker nipradilol on synthesis⁄repair cells this NOS blockaded SHR. Twenty-week-old SHR were administered inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 80 mg/l drinking water) or co-treated same dose L-NAME (20 mg/kg/day) 3 weeks. After treatment, expression apoptosis histologically examined using caspase-3, inducer, addition PCNA (DNA synthesis/repair), examination morphometric changes, including number tuft area. Nipradilol reduced blood pressure preserved creatinine clearance reduction L-NAME/SHR. These associated normalization index caspase-3 score, index, increases numbers area, resulting a decreased injury score. Thus, improved association decrease synthesis/repair cells. findings may provide important insights into repair/repair nephrosclerosis. (Hypertens Res 2002; 25: 433-440)