Endothelin and XXXX .

@entity1 @entity8 @entity295 @entity5409 @entity63 @entity4295 @entity1627 @entity810 @entity1986 @entity2231
UNASSIGNED: All components of the endothelin (ET) system are present in renal tubular cells. In this review, we summarize current knowledge about ET and the most common tubular diseases: @entity810 ( @entity810 ) and @entity8 . @entity810 originally was called @entity4295 , pointing to the most prominent morphologic findings. Similarly, cysts in @entity8 , and especially in @entity8 , are of tubular origin. Preclinical studies have indicated that the ET system and particularly @entity2231 receptors are involved in the pathogenesis of @entity63 -reperfusion injury, although these findings have not been translated to clinical studies. The ET system also has been implicated in radiocontrast-dye-induced @entity810 , however, ET-receptor blockade in a large @entity1 study was not successful. The ET system is activated in @entity295 models of @entity810 ; the effectiveness of ET blocking agents in preclinical studies is variable depending on the model and the ET-receptor antagonist used. Numerous studies have shown that the ET system plays an important role in the complex pathophysiology associated with @entity8 . However, results from selective targeting of ET-receptor subtypes in animal models of @entity8 have proved disappointing and do not support clinical trials. These studies have shown that a critical balance between @entity2231 and @entity1627 receptor action is necessary to maintain structure and function in the @entity5409 . In summary, ETs have been implicated in the pathogenesis of several renal @entity1986 , however, experimental animal findings have not yet led to use of ET blockers in @entity1 beings.
