UNASSIGNED: The present studies were performed to investigate whether the differences described between the two modalities for interruption of the renin-angiotensin- @entity1369 system (RAAS), angiotensin-converting enzyme inhibitors (ACE-I) and @entity7774 AT 1receptor antagonists (AIIA) result in differences in renoprotective efficacy in the @entity35 remnant kidney model. Male @entity35 with an initial body weight of 225-300 g, underwent 5/6 renal ablation and had radiotransmitters installed for radiotelemetric blood pressure (BP) measurements, owing to the known limitations of periodic tail-cuff BP measurements to adequately reflect ambient BP profiles. After renal ablation surgery, the @entity35 received no treatment (n=10); @entity4688 (n=11) or @entity1564 (n=9) after the first week, both administered initially at a dose of 50 mg/l of drinking water (~10 mg/kg). However, the dose of @entity1564 had to be reduced to 10-25 mg/l in 4/9 @entity35 to avoid excessive @entity551 . Both @entity4688 and @entity1564 produced significant reductions in average systolic BP during the subsequent approximately six weeks of observations as compared with untreated @entity35 (187  4 mmHg, p<0.001), but @entity1564 was significantly more effective at these relative doses (121  3 vs. 133  4 mmHg, p<0.05). At approximately seven weeks, serum @entity1011 and @entity644 were measured before sacrifice for morphologic assessment of percentage @entity631 ( @entity631 ). Despite the described differences between ACE-I and AIIA after acute administration, the percentage @entity631 was reduced similarly by @entity4688 (down to 6.8  2.8%) and @entity1564 (down to 2.9  1.5%) as compared with untreated @entity35 (37.2  4.3%). Moreover, @entity631 in individual animals paralleled the BP reductions achieved. @entity644 was reduced in parallel to the decrease in % @entity631 . These data indicate that, at least in the 5/6 renal ablation model, RAAS blockade by either ACE-I or AIIA provides protection by BPdependent rather than BP-independent mechanisms. This may reflect the primarily @entity101 pathogenesis of @entity631 in this model, and the fact that @entity101 is also very @entity1808 -dependent in this model. Thus, these data suggest that models other than the 5/6 ablation model may be more appropriate to demonstrate the BP-independent protective effects of RAAS blockade.

Relative antihypertensive and glomeruloprotective efficacies of XXXX and candesartan cilexetil in the remnant kidney model.

@entity644 :: ('MESH:D011507', 'Disease') :: ['Proteinuria', 'proteinuria'] @entity4688 :: ('MESH:D004656', 'Chemical') :: ['enalapril'] @entity1369 :: ('MESH:D000450', 'Chemical') :: ['aldosterone'] @entity101 :: ('MESH:D006973', 'Disease') :: ['hypertension', 'hypertensive'] @entity7774 :: ('MESH:D000809', 'Chemical') :: ['angiotensin'] @entity631 :: ('MESH:D005921', 'Disease') :: ['GS', 'glomerulosclerosis'] @entity1808 :: ('24179(Tax:10116)', 'Gene') :: ['angiotensin II'] @entity1564 :: ('MESH:C081643', 'Chemical') :: ['candesartan'] @entity1011 :: ('MESH:D003404', 'Chemical') :: ['creatinine'] @entity35 :: ('10116', 'Species') :: ['rat', 'Sprague-Dawley rats', 'rats'] @entity551 :: ('MESH:D007022', 'Disease') :: ['hypotension']
@entity4688 :: (MESH:D004656,Chemical) :: ['enalapril']
