Does XXXX reduce renal function in renovascular disease by postglomerular vasodilatation?

@entity1 @entity1289 @entity101 @entity1421 @entity384 @entity1854 @entity3371 @entity2791 @entity810 @entity916
In @entity101 @entity1 with @entity2791 ( @entity2791 ) or @entity2791 of a solitary kidney, reversible decrease of glomerular filtration rate (GFR) or @entity810 has been observed following @entity3371 administration. Decrease of GFR has been ascribed to preferential efferent vasodilatation. To test this hypothesis, acute changes of mean arterial pressure (MAP), renal plasma flow (RPF), GFR, plasma @entity916 activity (PRA) and @entity1421 -excretion after 50 mg @entity3371 orally were measured in post-transplant hypertensives with and without transplant @entity2791 (TRAS) during treatment with diuretics. The fall in MAP was similar in both groups; RPF did not change significantly; GFR decreased from 58 +/- 14 (s.d.) to 49 +/- 14 ml/min (TRAS, n = 8) and from 60 +/- 15 to 50 +/- 16 ml/min (without TRAS, n = 8). There was no evidence of @entity384 in @entity1 with TRAS, and filtration fraction decreased only in @entity1 without TRAS. Increase of PRA after @entity3371 was not significantly different between the two groups. @entity1421 -excretion did not change significantly. In one @entity1 with severe TRAS, long term @entity1289 ( @entity1289 ) inhibition and acute normalization of MAP with @entity1854 both induced a comparable decrease of GFR. The results demonstrate that acute postglomerular vasodilatation does not necessarily occur after @entity1289 inhibition in @entity1 with TRAS and a high- @entity916 state.
