Restriction of placental and fetal growth in sheep alters fetal blood pressure responses to angiotensin II and captopril

Edwards, L. J.; Simonetta, Giuseppe; Owens, Julie A.; Robinson, Jeffrey S.; McMillen, I. Caroline

doi:10.1111/j.1469-7793.1999.897ab.x

Cited by 123 publications

(160 citation statements)

References 33 publications

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“…However, this period of elevated plasma renin activity corresponded to a relative hypotension in the IUGR lambs; this raises the possibility that the increased plasma renin activity was a response to the lower arterial pressure. A recent study (30) found no difference in the MAP of control and IUGR fetuses (following carunclectomy); however, these two groups of animals responded differently to captopril (ACE inhibitor) and angiotensin II infusions. These results (30) suggest that arterial pressure in IUGR fetuses may be regulated by the renin-angiotensin system in a manner different to that in normal fetuses.…”

Section: Discussionmentioning

confidence: 99%

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

et al. 2000

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Low birth weight has been associated with elevated arterial pressure in later life but mechanisms are unknown. Our aim was to determine the effects of low birth weight resulting from intrauterine growth restriction (IUGR) on fetal and postnatal arterial pressures and the potential roles of circulating cortisol and renin. We induced IUGR by umbilico-placental embolization (UPE) in fetal sheep from 120 d of gestation until birth (approximately 147 d); postnatal lambs (8 IUGR, 8 controls) were studied for 8 wk. Fetal and postnatal arterial pressures were measured and blood samples taken for measurement of gas tensions, cortisol concentrations and renin activity. In IUGR fetuses, mean arterial pressure (MAP) initially increased with UPE, but near term was not different to values in controls. IUGR lambs weighed 33% less than controls at birth and remained lighter than controls during the 8 postnatal weeks; their growth pattern was different to that of controls. IUGR lambs had lower MAP than controls, and this relative hypotension (Ϫ4 mm Hg) persisted throughout the 8 postnatal weeks. Covariate analysis showed that the relative hypotension of IUGR lambs could have resulted from their smaller size. Plasma cortisol concentrations were not different between IUGR and control animals before or after birth. Plasma renin activity was not different in postnatal IUGR lambs compared with controls. Thus, postnatal cortisol and renin levels were not consistent with the development of hypotension or hypertension. We conclude that late gestational IUGR in sheep leads to relative hypotension in the early postnatal period, probably a result of reduced body size. There is increasing evidence that low birth weight resulting from intrauterine growth restriction (IUGR) is associated with an increased risk of later illness. Associations have been demonstrated between low birth weight and an increased risk of adult-onset diseases such as hypertension, coronary heart disease and type II diabetes (1, 2). In adults, an inverse relationship has been found between arterial pressure and birth weight (3, 4) and this relationship has been found to be independent of current body size and lifestyle factors (1). Studies in children have also revealed inverse relationships between birth weight and arterial pressure (5). The relationship in adolescents is less clear with some studies finding inverse relationships between birth weight and arterial pressure (6) and others finding positive relationships (7). Based on epidemiologic findings, it has been proposed that hypertension is initiated in utero and is amplified with age (8).Several studies of fetal growth restriction in animals have also shown relationships between a sub-optimal intrauterine environment and arterial pressure. Mid-gestational uterine artery ligation in guinea pigs has been shown to produce growth restricted offspring with an elevated mean arterial pressure (9). In the rat, a low protein diet during pregnancy also leads to growth restricted offspring with an elevated systolic pressure...

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Section: Discussionmentioning

confidence: 99%

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

et al. 2000

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“…Pentothal; Rhone Merieux, Pinkenba, Qld Australia) and maintained with halothane (2.5-4% Fluothane; ICI, Melbourne, Vic, Australia) in oxygen. Vascular catheters were inserted into a fetal carotid artery and jugular vein, the maternal jugular vein and into the amniotic cavity as previously described (Edwards et al 1999). Vascular catheters were inserted into one fetus in twin pregnancies.…”

Section: Embryo Transfer and Pregnancy Monitoringmentioning

confidence: 99%

Somatic cell nuclear transfer in the sheep induces placental defects that likely precede fetal demise

Fletcher¹,

Roberts²,

Hartwich³

et al. 2007

Reproduction

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The efficiency of cloning by somatic cell nuclear transfer (SCNT) is poor in livestock with w5% of transferred cloned embryos developing to term. SCNT is associated with gross placental structural abnormalities. We aimed to identify defects in placental histology and gene expression in failing ovine cloned pregnancies to better understand why so many clones generated by SCNT die in utero. Placentomes from SCNT pregnancies (nZ9) and age matched, naturally mated controls (nZ20) were collected at two gestational age ranges (105-134 days and 135-154 days; termZ147 days). There was no effect of cloning on total placental weight. However, cloning reduced the number of placentomes at both gestational ages (105-134 days: control 55.0G4.2, clone 44.7G8.0 and 135-154 days: control 72.2G5.1, clone 36.6G5.1; P!0.001) and increased the mean individual placentome weight (105-134 days: control 10.6G1.3 g, clone 18.6G2.8 g and 135-154 days: control 6.6G0.6 g, clone 7.0G2.0 g; P!0.02). Placentomes from cloned pregnancies had a significant volume of shed trophoblast and fetal villous hemorrhage, absent in controls, at both gestational age ranges (P!0.001) that was shown to be apoptotic by activated caspase-3 immunoreactivity. Consequently, the volume of intact trophoblast was reduced and the arithmetic mean barrier thickness of trophoblast through which exchange occurs was altered (P!0.001) at both gestational age ranges in clones. In addition, cloning reduced placental expression of key genes in placental differentiation and function. Thus, cloning by SCNT results in both gross and microscopic placental abnormalities. We speculate that trophoblast apoptosis, shedding, and hemorrhage may be causal in fetal death in ovine clones. Reproduction (2007) 133 243-255

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“…In fetal and neonatal sheep, hemorrhage and hypovolemia increase circulating angiotensin II (Ang II) (5)(6)(7). Although inhibition of Ang II receptors (AT) or converting enzyme accentuates hypovolemic episodes (3,7), their effects on basal arterial pressure are inconsistent (8,9). AT blockade also modifies the baroreflex and reflex control of renal sympathetic nerve activity after birth (10,11).…”

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confidence: 99%

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

et al. 2005

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Umbilical and systemic responses to angiotensin II differ in term fetal sheep, and peripheral vascular responses are attenuated or absent before and after birth. These observations may reflect developmental differences in angiotensin II receptor (AT) subtypes in vascular smooth muscle (VSM). Studies of AT subtype ontogeny and regulation are generally limited to the aorta, which may not be extrapolated to other arteries, and neither is completely described during ovine development. We therefore characterized VSM AT subtype expression and regulation throughout an extended period of development in umbilical and carotid artery and aorta from fetal (85-146 d gestation), postnatal (5-23 d), and adult sheep, measuring AT 1 and AT 2 mRNA and protein and performing immunohistochemistry. Parallel increases in umbilical AT 1 mRNA and protein began early in gestation and continued to term, and although AT 2 mRNA was unchanged, protein levels decreased Ͼ90% at term. Fetal carotid AT 1 mRNA was Ͻ40% of adult values and unchanged before birth; however, AT 1 protein rose Ͼ2-fold at term. After birth, AT 1 mRNA increased to 85% of adult values and was associated with another 2-fold rise in protein. In contrast, carotid AT 2 mRNA and protein fell in parallel throughout development and were barely detectable in the newborn and the adult. Immunostaining was consistent with observations in both arteries. A third pattern occurred in aortic VSM. The ontogeny of AT subtype expression and regulation is vessel specific, with changes in umbilical VSM beginning very early in development. Although the mechanisms that regulate mRNA and protein expression are unclear, these changes parallel differences in VSM maturation and function and local blood flow. The renin-angiotensin system (RAS) is expressed early in gestation and considered an important modulator of cardiovascular development, adaptation, and blood pressure control before and after birth (1-4). In fetal and neonatal sheep, hemorrhage and hypovolemia increase circulating angiotensin II (Ang II) (5-7). Although inhibition of Ang II receptors (AT) or converting enzyme accentuates hypovolemic episodes (3,7), their effects on basal arterial pressure are inconsistent (8,9). AT blockade also modifies the baroreflex and reflex control of renal sympathetic nerve activity after birth (10,11). Recent evidence suggests the RAS also contributes to the differentiation, maturation, and/or growth of vascular smooth muscle (VSM) (12-15). Thus, prevailing evidence suggests the RAS contributes to the regulation of vascular function, maturation, and growth during development.The effects of the RAS are mediated primarily by Ang II activation of ATs, which belong to the superfamily of seven transmembrane receptors (12,16,17). They are present in mammalian fetal and adult VSM and demonstrate similar binding characteristics during development and in the adult (18 -20). In fetal sheep, AT binding density and affinity in aorta and placental arteries are unchanged in the last third of gestation and resemble ...

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Restriction of placental and fetal growth in sheep alters fetal blood pressure responses to angiotensin II and captopril

Cited by 123 publications

References 33 publications

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

Placental Insufficiency and Fetal Growth Restriction Lead to Postnatal Hypotension and Altered Postnatal Growth in Sheep

Somatic cell nuclear transfer in the sheep induces placental defects that likely precede fetal demise

Vessel-Specific Regulation of Angiotensin II Receptor Subtypes During Ovine Development

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