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Perinatal growth disturbance in the spontaneously hypertensive rat
R M Lewis1, D C Batchelor, N S Bassett
1Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand.
Insights
Spontaneously hypertensive rats (SHR) exhibit disproportionate fetal and placental growth, altered metabolism, and endocrine differences compared to Wistar-Kyoto rats, suggesting abnormal perinatal physiology that may contribute to hypertension development.
Area of Science:
- Perinatal physiology
- Developmental biology
- Hypertension research
Background:
- Disproportionate fetal and placental growth are linked to hypertension in rats and humans.
- The spontaneously hypertensive rat (SHR) is a genetic model for human essential hypertension.
- Understanding perinatal differences in SHR is crucial for hypertension research.
Purpose of the Study:
- To investigate fetal, neonatal, and placental growth differences between SHR and Wistar-Kyoto (WKY) rats.
- To analyze metabolic and endocrine variations in SHR fetuses and neonates.
- To explore the relationship between perinatal abnormalities and the development of hypertension in SHR.
Main Methods:
- Comparative analysis of fetal and placental growth parameters in SHR and WKY rat strains.
- Assessment of metabolic markers including blood glucose, lactate, and hematocrit in fetuses.
- Evaluation of endocrine factors such as Insulin-like Growth Factor (IGF) and IGF-binding protein 2 (IGFBP-2) in SHR and WKY.
Main Results:
- SHR exhibited longer gestation, lower fetal and neonatal body weights, and significantly larger placentas compared to WKY.
- SHR neonates showed cardiac and renal hypertrophy, and a decreased ponderal index.
- SHR fetuses displayed lower blood glucose, higher blood lactate, reduced hematocrit, and decreased fetal liver IGFBP-2 mRNA and plasma IGFBP-2 levels.
Conclusions:
- SHR fetuses may experience undernutrition and placental insufficiency.
- Abnormal perinatal physiology, including altered growth and metabolic/endocrine parameters, is evident in SHR.
- These perinatal differences in SHR suggest a potential influence on the later development of hypertension.
Abstract:
Disproportionate fetal and placental growth are associated with the development of hypertension in the rat and human. Here we report differences in fetal, neonatal, and placental growth, and in metabolism and endocrinology, between the spontaneously hypertensive rat (SHR), a genetic model for human essential hypertension, and the control Wistar-Kyoto (WKY) strain. Gestation in SHR (23 d) was longer than in WKY by 20 h. Body weights were lower in the SHR from fetal d 16 to 20 and on postnatal d 15. However, on fetal d 22 and postnatal d 1, there was no significant difference in body weight between SHR and WKY. SHR placentas were larger than those of WKY at d 20, and by term there was a difference of 30% (p < 0.01). Other indices of disproportionate growth were hypertrophy of the fetal heart and kidney and decreased ponderal index in the SHR neonate. Blood glucose in SHR fetuses was lower than in WKY fetuses (p < 0.05), whereas blood lactate was higher (p < 0.05) and fetal hematocrit was reduced (p < 0.001). These findings suggest undernutrition and placental insufficiency may occur in SHR fetuses. Plasma IGF-II was increased on the last day of gestation in both strains, whereas IGF-I was unaltered. Fetal liver IGFBP-2 mRNA and plasma IGFBP-2 levels were reduced in SHR on fetal d 20 and 22 (p < 0.01). Differences in growth and endocrine and metabolic parameters suggest abnormal perinatal physiology in the SHR, which may influence the later development of hypertension.