XXXX augments ecto- @entity855 diphosphohydrolase activity and enhances endothelial anti-platelet function in @entity1 umbilical vein endothelial cells.

@entity1 @entity32 @entity1423 @entity5 @entity39 @entity310 @entity1564 @entity4770 @entity842 @entity1129 @entity2071 @entity715 @entity13796 @entity65 @entity855 @entity4687
OBJECTIVES: Recent clinical trials have demonstrated that angiotensin-converting enzyme inhibitors (ACEIs) reduce @entity715 events by unknown mechanisms in @entity1 with @entity65 . DESIGN: We studied the in-vitro effects of @entity4687 , an ACEI, on the ability of @entity1 umbilical vein endothelial cells (HUVEC) to inhibit @entity1423 . METHODS: Platelet aggregation in the presence of HUVEC and endothelial surface expression and activities of ecto- @entity855 diphosphohydrolase (ecto-ADPase), @entity13796 , were determined. The capability of HUVEC to release @entity4770 and @entity842 (NO) was also investigated. RESULTS: Perindoprilat (an active metabolite of @entity4687 ) significantly enhanced the surface expression and activities of ecto-ADPase and @entity4770 release, resulting in enhancement of ability to inhibit @entity1423 by HUVEC. These effects of perindoprilat were also observed in HUVEC activated by @entity5 @entity39 factor ( @entity310 , which increased the expression of @entity2071 ( @entity2071 ), @entity2071 , and, despite up-regulation of @entity4770 release, attenuated endothelial anti-platelet properties by decreasing ecto-ADPase activity. Perindoprilat partially restored this capability, but failed to reduce enhanced expression of @entity2071 . By contrast, the role of NO as a platelet inhibitor appeared minimal in HUVEC. @entity1564 , an angiotensin II receptor ( @entity1129 (1)) blocker, did not affect endothelial anti-platelet property. CONCLUSIONS: Perindoprilat was found to augment endothelial capability to inhibit @entity1423 by increasing ecto-ADPase activity and @entity4770 release in HUVEC. This beneficial effect of perindoprilat appeared to be preserved in the activated cells exposed to @entity310 , although no evidence was found to support that it could reverse the @entity32 process induced by cytokines.
