Fetal growth retardation and increased placental weight in the spontaneously hypertensive rat
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1Department of Paediatrics, University of Auckland, New Zealand.
Insights
Hypertension risk in adults is linked to fetal growth. This study in genetically hypertensive rats shows reduced fetal weight and increased placental weight, suggesting genetic factors influence these traits and hypertension development.
Area of Science:
- Developmental Biology
- Cardiovascular Physiology
- Genetics
Background:
- Epidemiological studies associate low birth weight and high placental weight with adult hypertension.
- Intrauterine growth retardation is proposed to initiate cardiovascular changes leading to hypertension.
- Genetic influences on fetal/placental size and hypertension are less understood due to human birth weight variability.
Purpose of the Study:
- To investigate the relationship between genetic hypertension and fetal/placental weight in a rat model.
- To explore potential genetic determination of fetal growth retardation and placental size in hypertension.
Main Methods:
- Comparison of fetal and placental weights at Day 20 gestation in spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) controls.
- Measurement of maternal blood pressure, blood glucose, and plasma insulin concentrations in SHR and WKY dams.
- Analysis of litter size to control for potential confounding factors.
Main Results:
- SHR fetuses were significantly smaller (reduced fetal weight) than WKY fetuses.
- SHR placentas were significantly heavier than WKY placentas, despite similar litter sizes.
- SHR dams exhibited higher blood pressure, elevated blood glucose, and lower plasma insulin compared to WKY dams.
Conclusions:
- The findings support human studies linking adult hypertension with a reduced fetal:placental weight ratio.
- In the genetically hypertensive rat model, fetal growth retardation and increased placental weight appear to be genetically determined.
- This suggests a potential genetic basis for the observed associations between early-life growth parameters and adult hypertension.
Abstract:
Epidemiological studies have linked low birth weight and increased placental weight with increased risk of hypertension in adult life. It has been proposed that the cardiovascular changes which lead to hypertension are initiated in utero by processes associated with intrauterine growth retardation. The alternative possibility, that hypertension may result from genetic influences which also determine fetal and placental size, has had less support because birth weight is not determined genetically in humans. However, in the spontaneously hypertensive rat (SHR) essential hypertension is known to be transmitted genetically. Fetal and placental weights were, therefore, measured at Day 20 gestation in SHRs and compared with those in the normotensive Wistar Kyoto (WKY) control strain. Fetal weight (1.93 +/- 0.04 g) was significantly (P < 0.001) reduced in SHRs compared with WKY fetuses (2.23 +/- 0.01 g) but placental weight was heavier (P < 0.001) in SHRs (0.347 +/- 0.005 g) than in WKY rats (0.300 +/- 0.006 g) although litter size was not different. As expected, maternal blood pressure recorded under 1% halothane anaesthesia was higher (126 +/- 2.7 mm Hg) in SHR than WKY rats (100 +/- 2.1 mm Hg; 1 mm Hg = 133 Pa). In addition the concentration of maternal blood glucose in SHR was significantly (P < 0.001) higher (4.8 +/- 0.32 mM v. 3.7 +/- 0.11 mM) and the concentration of plasma insulin was significantly (P < 0.05) lower in SHRs (18.8 +/- 3.0 ng mL-1) than in WKY dams (29.4 +/- 3.1 ng mL-1). Thus, the data support human population studies which show an association between adult hypertension and a reduced fetal:placental weight ratio at birth. However, because hypertension in the SHR is genetically determined, these data suggest that fetal growth retardation and increased placental weight may also be determined genetically.