An adenosine agonist, AMP-activated protein kinase (AMPK) activator and K ATP channel opener all caused bradycardia in normoxic conditions however, putative antagonists for these systems failed to prevent or ameliorate hypoxia-induced bradycardia. Oxygen concentrations ≤60% caused a concentration-dependent decrease in HR from normal levels of ~210 bpm. Utilizing a whole-embryo culture technique, we examined the effects of different pharmacological agents on HR under normoxic (95% oxygen) and hypoxic (20% oxygen) conditions. The gestational day 13 rat embryo is a good model for the human embryo at 5–6 weeks gestation, as the heart is comparable in development and, like the human embryo, has no functional autonomic nerve supply at this stage. The aim of this study was to gain insight into whether the first trimester embryo could control its own heart rate (HR) in response to hypoxia.
