The main findings include: (a) prenatal hypoxia plus postnatal HF diets significantly exacerbated plasma lipid concentrations compared with the HF‐fed only; (b) prenatal hypoxia exacerbated HF‐elevated BP and vascular tone via up‐regulated α1c‐subunits, resulting in increased Cav1.2 channel currents; (c) postnatal HF caused up‐regulated BK β1‐subunits, leading to increased BK channel currents, independent of prenatal hypoxia (Figure 6). The gene discussed is CACNA1C; the disease is hydrops fetalis.