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Antenatal maternal long-term hypoxia (LTH) can alter serotonin (5-HT) and calcium (Ca²⁺) signaling in fetal pulmonary arteries (PAs) and is associated with persistent pulmonary hypertension of the newborn (PPHN). In humans, the antenatal maternal hypoxia can be secondary to smoking, anemia, and chronic obstructive pulmonary disorders. However, the mechanisms of antenatal maternal hypoxia-related PPHN are unresolved. Because both LTH and 5-HT are associated with PPHN, we tested the hypothesis that antenatal maternal LTH can increase 5-HT-mediated PA contraction and associated extracellular Ca²⁺ influx through L-type Ca²⁺ channels (Ca_L), nonselective cation channels (NSCCs), and reverse-mode sodium–calcium exchanger (NCX) in the near-term fetus. We performed wire myography and confocal-Ca²⁺ imaging approaches on fetal lamb PA (∼140 days of gestation) from normoxic ewes or …