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Programmed hypertension: kidney, brain or both?
Miodrag Dodic1, Karen Moritz, Irene Koukoulas
1Howard Florey Institute, University of Melbourne, Parkville, Victoria 3052, Australia. m.dolic@hfi.unimelb.edu.au
Trends in Endocrinology and Metabolism: TEM
|October 9, 2002
Summary
Prenatal exposure to excess glucocorticoids (GC) can lead to low birth weight and adult hypertension. This study proposes that permanent changes in fetal kidney and brain gene expression due to excess GC exposure are key factors in developing high blood pressure later in life.
Area of Science:
- Developmental biology
- Endocrinology
- Cardiovascular science
Background:
- Epidemiological studies link low birth weight to adult hypertension.
- Excess prenatal glucocorticoid (GC) exposure is an identified determinant.
- Hypertension develops in animal models exposed to excess GC during critical fetal development periods.
Purpose of the Study:
- To investigate the role of prenatal glucocorticoid (GC) exposure in the development of adult-onset hypertension.
- To propose that permanent alterations in fetal kidney and brain gene expression are critical mechanisms.
Main Methods:
- Utilizing animal models (sheep and rats) exposed to excess GC during gestation.
- Examining kidney and brain development at critical fetal stages.
- Assessing adult offspring for hypertension development.
Main Results:
- Prenatal GC exposure in animal models resulted in hypertension in adulthood.
- These effects were observed when exposure occurred during early fetal development when kidneys and brain are primitive.
- Suggests a link between early developmental programming and later-life disease.
Conclusions:
- Prenatal exposure to excess glucocorticoids (GC) is implicated in adult-onset hypertension.
- Permanent changes in fetal gene expression and function in the kidney and brain are proposed as crucial mechanisms.
- This highlights the long-term consequences of the prenatal environment on cardiovascular health.