An activated renal endothelin (ET) system is implicated in the pathogenesis of @entity8 , as recently shown in ET-1 @entity19 . Because progressive @entity8 is also a major finding in @entity2316 , we analyzed the activity of the renal ET system in @entity35 with @entity3839 -induced @entity6 and the effect of blocking the ETA receptor, using the orally active ETA antagonist @entity32593 . The effects of long-term treatment with @entity32593 were compared with those of an @entity1811 inhibitor. Plasma and urinary ET-1 concentrations were measured. Progression of @entity2316 was analyzed by measuring urinary albumin and protein excretion. Urinary ET-1 excretion was significantly elevated as early as 7 days after induction of @entity6 and increased further. The daily urine volume was significantly correlated with urine ET-1 excretion. Treatment with @entity32593 significantly decreased the ET-1 excretion by more than 50%, whereas @entity1811 inhibition resulted only in a mild decrease. Albumin excretion was significantly decreased after @entity1811 inhibition, whereas ETA inhibition resulted in a nonsignificant decrease. Urinary ET and albumin excretion probably reflect independent mechanisms of @entity8 in @entity6 .

Renal endothelin system in XXXX : comparison of angiotensin-converting enzyme inhibition and endothelin-A antagonism.

@entity1811 :: ('24310(Tax:10116)', 'Gene') :: ['ACE'] @entity8 :: ('MESH:D007674', 'Disease') :: ['renal fibrosis', 'renal damage'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetes', 'diabetes mellitus'] @entity19 :: ('10090', 'Species') :: ['transgenic mice'] @entity2316 :: ('MESH:D003928', 'Disease') :: ['diabetic nephropathy'] @entity3839 :: ('MESH:D013311', 'Chemical') :: ['streptozotocin'] @entity35 :: ('10116', 'Species') :: ['rats'] @entity32593 :: ('MESH:C107831', 'Chemical') :: ['LU 135252']
@entity6 :: (MESH:D003920,Disease) :: ['diabetes']
