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The selfish brain and the barker hypothesis.

E R Lumbers1, Z Y Yu, K J Gibson

  • 1School of Physiology and Pharmacology, University of New South Wales, Sydney, New South Wales, Australia. e.lumbers@unsw.edu.au

Clinical and Experimental Pharmacology & Physiology
|November 13, 2001
PubMed
Summary

Intra-uterine growth retardation (IUGR) can lead to fewer nephrons, increasing the risk of adult hypertension. Fetal sympathetic nerve activity may negatively impact kidney development and nephron count.

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Area of Science:

  • Developmental Biology
  • Nephrology
  • Cardiovascular Physiology

Background:

  • Intra-uterine growth retardation (IUGR) is linked to reduced brain growth relative to body growth.
  • IUGR and low birth weight are associated with increased risk of adult hypertension, cardiovascular disease, and diabetes mellitus.
  • Nephrogenesis, the formation of nephrons, is completed before birth in humans and shortly after birth in rats; both IUGR and undernutrition are associated with reduced nephron number.

Purpose of the Study:

  • To explore the relationship between fetal development, kidney development, and the sympathetic nervous system.
  • To understand how factors affecting fetal growth may predispose individuals to adult hypertension.
  • To investigate the role of the renin-angiotensin system (RAS) and renal sympathetic nerve activity (RSNA) in kidney development and long-term cardiovascular health.

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Main Methods:

  • Review of existing literature on IUGR, nephrogenesis, and the renin-angiotensin system.
  • Analysis of studies investigating the effects of RAS blockade and renal denervation on nephron number and blood pressure in animal models.
  • Examination of fetal sheep studies on renal sympathetic nerve activity and its determinants.

Main Results:

  • Oligonephropathy (reduced nephron number) may lead to hyperfiltration, glomerulosclerosis, and hypertension.
  • In rats, pharmacological blockade of the RAS in early life reduces glomerular number and causes adult hypertension.
  • Renal denervation in fetal rats affects RAS activity and renin-secreting cell development, potentially impacting blood pressure.
  • Fetal sheep exhibit tonic renal sympathetic nerve activity influenced by behavioral state.
  • High levels of fetal RSNA may cause vasoconstriction, limiting nephrogenesis and potentially predisposing to adult hypertension.

Conclusions:

  • Reduced nephron endowment due to IUGR or developmental factors is a potential mechanism for adult hypertension.
  • The developing sympathetic nervous system and the renin-angiotensin system interact during kidney development.
  • Fetal exposure to high sympathetic activity or RAS disruption could program for long-term cardiovascular risk.