Alterations in maternal diet during pregnancy have been shown to change fetal and postnatal growth and physiology; here, the sensitivity of early embryonic development to maternal diet was assessed. Virgin female MF-1 mice were mated and randomly assigned to one of three diets, (a) normal protein diet of 18% casein (NPD), (b) isocaloric low protein diet of 9 % casein (LPD), or (c) LPD for the preimplantation period (3.5 days) then switched to NPD for the remainder of gestation (Emb-LPD). At birth, pups were weighed and litter size adjusted to a mean of 3 males, 3 females. Offspring were weighted weekly thereafter. Offspring behavioural patterns were assessed using an open field test. Blood pressure measurements were recorded using tail cuff. At 22 weeks, male mesenteric arteries were mounted on a wire myograph and the vasoreactivity of the vessels recorded. At 28 weeks, offspring were sacrificed, organs were weighed and stored. Female left kidneys were processed into glycol methacrylate and glomerular number determined using stereology. At birth, Emb-LPD females were significantly heavier than controls (p < 0.05). Egg-LPD females were significantly heavier than controls for several weeks up 28 weeks of age (p < 0.05). At 15 and 21 weeks of age, both male and female LPD and Emb-LPD offspring had a significantly elevated systolic blood pressure when compared to NPD offspring (p < 0.05). In myopgraphy, no significant differences were observed between male treatment groups. LPD females had significantly elevated serum angiotensin converting enzyme (ACE) activity, a know regulator of blood pressure through the generation of angiotensin II, a potent vasodilator. Emb-LPD and LPD females displayed significantly reduced heart:body weight ratios when compared to control females (p<0.05). Globally, Emb-LPD females showed significantly elevated open field activities (distance travelled and vertical counts), and significantly decreased time spent resting, when compared to controls (p ≤ 0.05). These data support the hypothesis that alterations in maternal diet during early embryonic development result in significantly altered pattens of postnatal growth, systolic blood pressure, and behaviour patterns.