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A Rat Model of Mild Intrauterine Hypoperfusion with Microcoil Stenosis
Published on: January 7, 2018
Prenatal dehydration alters renin-angiotensin system associated with angiotensin-increased blood pressure in young
Junchang Guan1, Caiping Mao, Feichao Xu
1Perinatal Biology Center, Soochow University First Affiliated Hospital, Suzhou, China.
Insights
Maternal dehydration during pregnancy alters fetal renin-angiotensin system (RAS) development, leading to increased blood pressure (BP) in offspring when exposed to angiotensin II. This highlights the impact of prenatal stress on cardiovascular regulation.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Endocrinology
Background:
- The renin-angiotensin system (RAS) is crucial for maintaining cardiovascular homeostasis.
- Maternal health during pregnancy significantly influences offspring development and long-term health outcomes.
- Understanding the impact of environmental stressors like dehydration on fetal RAS development is vital.
Purpose of the Study:
- To investigate the effects of maternal water deprivation during late gestation on the fetal renin-angiotensin system (RAS) in rats.
- To examine the influence of prenatal dehydration on the cardiovascular responses and blood pressure regulation in adolescent offspring.
- To assess changes in fetal and offspring cardiac angiotensin II receptor expression.
Main Methods:
- Pregnant rats were subjected to water deprivation for 3 days during late gestation.
- Fetal cardiac ultrastructure, liver angiotensinogen mRNA, plasma Ang I and Ang II, and cardiac AT(1) and AT(2) receptor mRNA and protein levels were analyzed.
- Cardiovascular responses to intravenous Angiotensin II infusion and baroreflex sensitivity were tested in adolescent offspring.
Main Results:
- Maternal water deprivation led to decreased fetal body and heart weight, increased fetal plasma sodium and osmolality.
- Fetal liver angiotensinogen mRNA and plasma Ang II concentrations were elevated.
- Prenatal dehydration increased fetal and offspring cardiac AT(2) receptor expression and resulted in elevated blood pressure in response to Ang II infusion in offspring.
Conclusions:
- Prenatal exposure to maternal dehydration significantly impacts the development of the renin-angiotensin system in fetal rats.
- This developmental alteration is associated with an increased blood pressure response to Angiotensin II in offspring.
- The study underscores the long-term cardiovascular consequences of prenatal dehydration on offspring physiology.
Abstract:
The renin-angiotensin system (RAS) has an important role in cardiovascular homeostasis. This study determined the influence of water deprivation during pregnancy on the development of the RAS in rats, and examined blood pressure (BP) in the adolescent offspring. Pregnant rats were water deprived for 3 days at late gestation, and we examined fetal cardiac ultrastructure, as well as heart angiotensin (Ang) II receptor protein and mRNA, liver angiotensinogen and plasma Ang II concentrations. We also tested cardiovascular responses to i.v. Ang II in the young offspring. In utero exposure to maternal water deprivation significantly decreased fetal body and heart weight, and increased fetal plasma sodium and osmolality. Fetal liver angiotensinogen mRNA, plasma Ang I and Ang II concentrations were also increased. Although fetal AT(1a) and AT(1b) receptor mRNA and AT(1) protein were not changed, AT(2) receptor mRNA and protein levels in the heart were significantly increased following maternal dehydration. Prenatal exposure to maternal water deprivation had no effect on baseline BP; however, it significantly increased BP in response to i.v. Ang II infusion, and decreased baroreflex sensitivity in the offspring. In addition, the heart AT(2) receptor mRNA and protein were higher in the offspring exposed to prenatal dehydration. The results of this study demonstrate that prenatal dehydration affected the RAS development associated with an Ang II-increased BP in fetal origin.
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