β-Adrenergic receptor (βAR) activation has been shown to maintain heart rate during hypoxia and to rescue the fetus from the fetal lethality that occurs in the absence of norepinephrine. This study examines whether the same subtype of βAR is responsible for survival and heart rate regulation. It also investigates which βARs are located on the early fetal heart and whether they can be directly activated during hypoxia. Cultured E12.5 mouse fetuses were treated with subtype-specific βAR antagonists to pharmacologically block βARs during a hypoxic insult. Hypoxia alone reduced heart rate by 35–40% compared to prehypoxic levels. During hypoxia, heart rate was further reduced by 31% in the presence of a β1AR antagonist, CGP20712A, at 100 nM, but not with a β2 (ICI118551)- or a β3 (SR59230A)-specific antagonist at 100 nM. Survival in utero was also mediated by β1ARs. A β1 partial agonist, xamoterol, rescued 74% of catecholamine-deficient (tyrosine-hydroxylase-null) pups to birth, a survival rate equivalent to that with a nonspecific βAR agonist, isoproterenol (87%). Receptor autoradiography showed that β1ARs were only found on the mouse heart at E12.5, while β2ARs were localized to the liver and vasculature. To determine if the response to hypoxia was intrinsic to the heart, isolated fetal hearts were incubated under hypoxic conditions in the presence of a βAR agonist. Heart rate was reduced to 25–30% by hypoxia alone, but was restored to 63% of prehypoxic levels with 100 nM isoproterenol. Restoration was completely prevented if β1ARs were blocked with CGP20712A at 300 nM, a concentration that blocks β1ARs, but not β2- or β3ARs. Our results demonstrate that β1ARs are located on the heart of early fetal mice and that β1AR stimulation maintains fetal heart rate during hypoxia and mediates survival in vivo.