Do elevated endothelin-1 levels impair nitric oxide homeostasis through a PKC-dependent pathway?
Our study demonstrates that high levels of ET-1 impair endothelial NO production via an isoform-specific PKC-mediated inhibition of eNOS expression. ET-1 antagonism with bosentan stimulates translocation of PKClambda and leads to increased PKC activity and NO production. ET-1 antagonism may provide a novel therapeutic strategy to improve vascular homeostasis.
G6PD deficiency offers an explanation for idiopathic priapism. The medical condition generates a pathophysiologic milieu consistent with aberrant NO signaling and heightened oxidative stress in the penis.