Nitric oxide (NO) has been linked to a number of embryonic processes, yet the role of nitric oxide signalling in development remains largely unknown. Dimethylarginine dimethylaminohydrolase 1 (DDAH1) catalyzes the breakdown of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide production, and may also have nitric oxide-independent functions. We generated transgenic mice targeting the DDAH1 locus. The recent characterization of these mice indicated that homozygous deletion of DDAH1 appeared lethal in utero. Moreover, the loss of DDAH1 activity in DDAH1^+/- mice leads to a reduction in NO signalling and consequently vascular dysfunction. Here we report that DDAH1 null embryos are fertilised at low frequency: 4 DDAH1^-/- blastocysts detected in 79 scored (5.1%). Furthermore, the null embryos fail to undergo uterine implantation and are thus non-viable. In addition, DDAH1^+/- females have a high frequency of embryo resorption (21 resorbing embryos of 73 scored (28.2%)). To elucidate an underlying role for DDAH1 which could explain these phenomena we documented its presence in the embryo. DDAH1 RNA is expressed in the left ventricle, cardiac outflow tract, developing vasculature, and developing limb buds. This pattern overlaps with the RNA expression pattern of the nitric oxide synthase (NOS) isoforms, and with NOS activity. Our data suggests that DDAH1 is necessary during several phases of embryonic development, possibly through specific effects on NO pathways.