Placental imbalance of vasoactive factors does not affect pregnancy outcome in XXXX treated with @entity205 after transplantation.

@entity1 @entity8 @entity9554 @entity101 @entity2232 @entity1110 @entity205 @entity842 @entity3623
@entity2232 ( @entity2232 ) and @entity842 (NO) have been suggested to have a focal role in the regulation of placental and fetal growth. @entity205 (CsA) has been shown to strongly modulate @entity2232 and NO synthesis and thus has the potential to affect fetal growth and maternal state. Eleven CsA-treated female kidney transplant recipients were recruited. Fourteen healthy pregnant @entity1 served as controls. Placental expression of @entity2232 and tissue factor (TF) was evaluated by in situ hybridization, and @entity3623 ( @entity3623 ) was evaluated by staining with the reduced form of @entity1110 ( @entity1110 )-diaphorase and in situ hybridization. Kidney transplant recipients showed a marked reduction in @entity1110 -diaphorase staining, as well as endothelial constitutive @entity3623 ( @entity9554 ) messenger RNA, whereas inducible @entity3623 expression was unchanged. Normal placenta showed a strong positive @entity2232 signal along the endothelium of uteroplacental arteries within the basal plate, which increased markedly in decidua of transplant recipients. Thus, transplant recipients showed a remarkable alteration in @entity2232 / @entity9554 balance without alteration in fetal growth or maternal renal function. Next, we explored the state of placental endothelial cell activation downstream from vasoactive factors by evaluating TF gene expression. Transplant recipients did not show modification of TF transcript compared with healthy pregnant @entity1 . CsA potently affected the placental @entity2232 / @entity9554 vasoactive balance. Nevertheless, newborns from transplant recipient mothers were appropriate for gestational age, and transplant recipients did not show systemic @entity101 or impending @entity8 . It is suggested that CsA may blunt the activation of endothelial cells and priming of endothelial-derived substances, which possibly lie downstream from the cited vasoactive agents.
