What happens in the womb during pregnancy can affect the short-term and long-term cardiovascular health of offspring. For example, pre-eclampsia — one of the leading causes of maternal and neonatal deaths worldwide — is known to increase the risk of cardiovascular disease in offspring. Moreover, this effect is heightened in women with pre-eclampsia and a background of chronic hypertension (a condition known as superimposed pre-eclampsia). The prevalence of pre-eclampsia is increasing, owing to the increasing number of pregnant women with pre-existing cardiovascular conditions (who are more likely to develop this condition); this highlights the need for more research into the mechanisms that are involved its development.

This model has been instrumental for investigating the long-term cardiovascular effects of ‘preeclampsia-like’ conditions on offspring through blood pressure and echocardiographic assessments from weaning up until adulthood. We have shown that offspring exposed to angiotensin II have increased left ventricular mass early in life, which leads to impaired cardiovascular function in their adulthood. In utero exposure to angiotensin II results in a decrease in fractional shortening and an increase in the ratio of early (E) to late (A) ventricular filling velocities between the ages of 9 and 17 weeks compared with controls, which are indicative of systolic and diastolic dysfunction, respectively. These results extend our understanding of cardiovascular development in utero and enable an exploration of the potential links between pre-eclampsia and the detrimental programming of the offspring. To summarize, this animal model has shown that an unfavourable in utero environment can shape the cardiovascular health of offspring later in life and has highlighted the importance of monitoring infants, children and adults who were born to mothers who had pre-eclampsia during pregnancy.