Abstract:Endothelial activation is critical to pulmonary vasorelaxation during the fetal transition. Bradykinin (BK) relaxes vessels through endothelial‐induced nitric oxide (NO) and prostacyclin (PGI2) dependent signaling pathways. Intrauterine long term hypoxia (LTH) can stunt vasorelaxation in the fetal transition and cause pulmonary hypertension of the newborn. We therefore tested the hypothesis that LTH impairs maturation of BK‐mediated vasorelaxation by performing wire‐myography on pulmonary arteries (PA) isolate… Show more
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