The release of NE from cardiac sympathetic nerve terminals is controlled by both presynaptic α2A- and α2CARs (Hein et al., 1999), and genetic deletion of both of these α2AR subtypes leads to cardiac hypertrophy and HF due to chronically enhanced cardiac NE release, as well as enhanced NE and Epi secretion from the adrenal medulla (Brede et al., 2002, 2003; Lymperopoulos et al., 2007). This evidence concerns the gene ADORA2A and hydrops fetalis.