The Fetal Origins of Hypertension

Funding Activity

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Funded Activity Summary

In the last ten years, a remarkable series of public health studies have shown that reduced birth weight is associated with an increased prevalence of high blood pressure, coronary heart disease, diabetes and obesity in adult life. These associations are independent of adult lifestyle or current size, are dependent on events initiated prenatally and are present in cohorts which have a birth weight distribution typical of urban and rural Australia. In all societies, the incidence of low birth weight babies has remained above 5% and in some developing countries, it is greater than 30%. The hormonal responses which help the fetus survive periods of growth restriction in utero, result in a permanent reprogramming of the development of key fetal organs and tissues and the subsequent emergence of high blood pressure in later life. The fetal hormones which have been implicated in causing high blood pressure in adult life are known as glucocorticoids. Fetuses may be exposed to excess glucocorticoids through stress in the womb or through increased transfer of glucocorticoids across the placenta. Currently 85% of Australian obstetricians prescribe repeat courses of antenatal corticosteroids in pregnancies in which the risk of preterm birth persists or recurs. The specific long term outcomes of fetal exposure to excess glucocorticoids are unknown and may depend on the timing, route, dose and type of glucocorticoids involved. We propose to define the mechanisms by which high levels of glucocorticoids act to result in high blood pressure and hormonal disturbances in adult life.

Funded Activity Details

Start Date: 01-01-2000

End Date: 01-01-2001

Funding Scheme: NHMRC Project Grants

Funding Amount: $129,431.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Public health nutrition

ANZSRC Socio-Economic Objective (SEO)

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Other Keywords

Developmental physiology | High blood pressure | Intrauterine growth restriction | Perinatal morbidity | Prenatal programming of high blood pressure | The fetal origins of adult disease