Abstract
A substantial number of epidemiological studies have shown that small size at birth is associated with an increased risk of developing hypertension and metabolic dysfunction later in life; however these associations have not been found in all studies. In animals, several models have been used to investigate the effects of perturbations to the fetal environment on later arterial pressure, with differing effects on size at birth and arterial pressure. Ovine models include maternal dietary manipulations, antenatal glucocorticoid exposure, and restriction of placental size and function. In our laboratory, we have induced late gestational placental insufficiency and growth restriction in sheep by umbilico-placental embolisation; during the early postnatal period the growth restricted lambs remained small and were hypotensive relative to controls. More recent long-term studies indicate that these growth restricted animals were able to catch up in body weight within the first postnatal year; however, their arterial pressure remained lower than that of controls throughout the first 2 postnatal years (AMAP, -4.2 ± 1.4 mmHg). This relative hypotension may be due to altered vascular or cardiac development resulting from increased vascular resistance or nutrient restriction during fetal life. As late gestational placental insufficiency led to a persistent reduction in arterial pressure from birth to adulthood, our findings do not support the hypothesis that restricted fetal growth per se leads to hypertension after birth. It is likely that the effects of a prenatal compromise on postnatal arterial pressure will vary depending on the nature of the associated developmental perturbations and their gestational timing.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 53-60 |
| Number of pages | 8 |
| Journal | Archives of Physiology and Biochemistry |
| Volume | 111 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 2003 |
| Externally published | Yes |
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Keywords
- Birth weight
- Blood pressure
- Fetal growth retardation
- Placental insufficiency
ASJC Scopus subject areas
- Physiology
- Biochemistry
Cite this
Postnatal development of arterial pressure : Influence of the intrauterine environment. / Louey, Samantha; Cock, M. L.; Harding, R.
In: Archives of Physiology and Biochemistry, Vol. 111, No. 1, 02.2003, p. 53-60.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Postnatal development of arterial pressure
T2 - Influence of the intrauterine environment
AU - Louey, Samantha
AU - Cock, M. L.
AU - Harding, R.
PY - 2003/2
Y1 - 2003/2
N2 - A substantial number of epidemiological studies have shown that small size at birth is associated with an increased risk of developing hypertension and metabolic dysfunction later in life; however these associations have not been found in all studies. In animals, several models have been used to investigate the effects of perturbations to the fetal environment on later arterial pressure, with differing effects on size at birth and arterial pressure. Ovine models include maternal dietary manipulations, antenatal glucocorticoid exposure, and restriction of placental size and function. In our laboratory, we have induced late gestational placental insufficiency and growth restriction in sheep by umbilico-placental embolisation; during the early postnatal period the growth restricted lambs remained small and were hypotensive relative to controls. More recent long-term studies indicate that these growth restricted animals were able to catch up in body weight within the first postnatal year; however, their arterial pressure remained lower than that of controls throughout the first 2 postnatal years (AMAP, -4.2 ± 1.4 mmHg). This relative hypotension may be due to altered vascular or cardiac development resulting from increased vascular resistance or nutrient restriction during fetal life. As late gestational placental insufficiency led to a persistent reduction in arterial pressure from birth to adulthood, our findings do not support the hypothesis that restricted fetal growth per se leads to hypertension after birth. It is likely that the effects of a prenatal compromise on postnatal arterial pressure will vary depending on the nature of the associated developmental perturbations and their gestational timing.
AB - A substantial number of epidemiological studies have shown that small size at birth is associated with an increased risk of developing hypertension and metabolic dysfunction later in life; however these associations have not been found in all studies. In animals, several models have been used to investigate the effects of perturbations to the fetal environment on later arterial pressure, with differing effects on size at birth and arterial pressure. Ovine models include maternal dietary manipulations, antenatal glucocorticoid exposure, and restriction of placental size and function. In our laboratory, we have induced late gestational placental insufficiency and growth restriction in sheep by umbilico-placental embolisation; during the early postnatal period the growth restricted lambs remained small and were hypotensive relative to controls. More recent long-term studies indicate that these growth restricted animals were able to catch up in body weight within the first postnatal year; however, their arterial pressure remained lower than that of controls throughout the first 2 postnatal years (AMAP, -4.2 ± 1.4 mmHg). This relative hypotension may be due to altered vascular or cardiac development resulting from increased vascular resistance or nutrient restriction during fetal life. As late gestational placental insufficiency led to a persistent reduction in arterial pressure from birth to adulthood, our findings do not support the hypothesis that restricted fetal growth per se leads to hypertension after birth. It is likely that the effects of a prenatal compromise on postnatal arterial pressure will vary depending on the nature of the associated developmental perturbations and their gestational timing.
KW - Birth weight
KW - Blood pressure
KW - Fetal growth retardation
KW - Placental insufficiency
UR - http://www.scopus.com/inward/record.url?scp=0037306586&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037306586&partnerID=8YFLogxK
U2 - 10.1076/apab.111.1.53.15137
DO - 10.1076/apab.111.1.53.15137
M3 - Article
C2 - 12715275
AN - SCOPUS:0037306586
VL - 111
SP - 53
EP - 60
JO - Archives of Physiology and Biochemistry
JF - Archives of Physiology and Biochemistry
SN - 1381-3455
IS - 1
ER -