Prevention or retardation of @entity2316 ( @entity2316 ) includes anti- @entity101 treatment with angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II type 1 receptor blockers ( @entity11882 ) on the premises that these drugs have an added protective effect beyond their influence on BP. The present study used a strain of spontaneously @entity101 /NIH-corpulent @entity35 [SHR/NDmc-cp (fat/fat)] as a model of type II @entity2316 to unravel the renoprotective effects of anti- @entity101 drugs. @entity9885 (1 or 5 mg/kg per d), an @entity11882 , and @entity2514 (5mg/kg per d), an anti- @entity101 drug without effect on the renin-angiotensin system (RAS), were given for 20 wk. BP, renal function, @entity413 and insulin levels, and @entity644 were monitored. @entity8 and kidney @entity23032 content were assessed at the end of the study. @entity9885 (1 and 5 mg) significantly reduced BP and kidney @entity23032 content and improved histologic @entity8 and @entity644 . The changes were dose-dependent. The effect of @entity2514 (5 mg) was similar to that of @entity9885 (1 mg) but reached statistical significance only for kidney @entity23032 content. The similarity of both drugs' effects on kidney damage and @entity644 suggest that renoprotection does not hinge on manipulation of RAS in these @entity35 . By contrast, the inhibition of renal @entity23032 formation assessed both by immunohistochemistry and HPLC suggests a critical role of advanced glycation end product (AGE) formation together with @entity101 in the genesis of @entity2316 . This view is supported by the correlation found between renal @entity23032 content and @entity644 . The unsuspected AGE-lowering effect of @entity2514 was further confirmed in vitro and elucidated; it is due to both reactive @entity6738 compounds trapping and modifications of the oxidative metabolism. It is concluded that AGE inhibition should be included in the therapeutic strategy of @entity2316 .

Anti- @entity101 agents inhibit in vivo the formation of advanced glycation end products and improve @entity8 in a type 2 XXXX @entity35 model.

@entity644 :: ('MESH:D011507', 'Disease') :: ['proteinuria'] @entity8 :: ('MESH:D007674', 'Disease') :: ['Glomerular lesions', 'renal damage'] @entity23032 :: ('CHEBI:59951', 'Chemical') :: ['pentosidine'] @entity101 :: ('MESH:D006973', 'Disease') :: ['hypertension', 'hypertensive'] @entity2316 :: ('MESH:D003928', 'Disease') :: ['diabetic nephropathy', 'DN'] @entity2514 :: ('MESH:D006830', 'Chemical') :: ['hydralazine'] @entity9885 :: ('MESH:C437965', 'Chemical') :: ['olmesartan', 'Olmesartan'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity11882 :: ('OMIM:611809', 'Disease') :: ['ARB'] @entity6738 :: ('CHEBI:23019', 'Chemical') :: ['carbonyl'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity2316 :: (MESH:D003928,Disease) :: ['diabetic nephropathy']
