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Prenatal Hypoxia Affects Foetal Cardiovascular Regulatory Mechanisms in a Sex- and Circadian-Dependent Manner: A
Hana Sutovska1, Katarina Babarikova1, Michal Zeman1
1Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, 842 15 Bratislava, Slovakia.
Insights
Prenatal hypoxia impacts cardiovascular development, leading to adult hypertension. These effects are influenced by circadian rhythms and can occur even with short-term exposure, independent of growth restriction.
Area of Science:
- Cardiovascular Physiology
- Developmental Biology
- Perinatal Medicine
Background:
- Prenatal hypoxia can disrupt fetal development, potentially causing adult hypertension.
- Intrauterine growth restriction often accompanies prenatal hypoxia, complicating analysis of hypoxia's independent effects.
- Understanding prenatal hypoxia's impact on cardiovascular regulation is crucial for long-term health outcomes.
Purpose of the Study:
- To analyze the effects of prenatal hypoxia, particularly when not associated with intrauterine growth restriction, on cardiovascular regulatory mechanisms.
- To investigate the roles of the placenta, maternal health, and environmental factors in prenatal hypoxia.
- To explore sex-dependent effects and the influence of circadian variability on prenatal hypoxia's cardiovascular programming.
Main Methods:
- Systematic review of publications up to September 2021.
- Focused analysis on cardiovascular regulatory mechanisms (chemoreflex, adenosine, nitric oxide, angiotensin II).
- Examined placental function, maternal/environmental factors, sex differences, and circadian variability.
Main Results:
- Prenatal hypoxia significantly affects cardiovascular regulatory mechanisms.
- Circadian variability and time of day influence the relationship between prenatal hypoxia and cardiovascular responses.
- Even short-term prenatal hypoxia can program hypertension in adulthood.
Conclusions:
- Prenatal hypoxia, even without intrauterine growth restriction, has lasting effects on cardiovascular regulation and hypertension risk.
- The timing and duration of prenatal hypoxia exposure, along with circadian factors, modulate its programming effects.
- Prenatal programming of hypertension is complex and influenced by multiple interacting factors including sex and circadian rhythms.
Abstract:
Prenatal hypoxia during the prenatal period can interfere with the developmental trajectory and lead to developing hypertension in adulthood. Prenatal hypoxia is often associated with intrauterine growth restriction that interferes with metabolism and can lead to multilevel changes. Therefore, we analysed the effects of prenatal hypoxia predominantly not associated with intrauterine growth restriction using publications up to September 2021. We focused on: (1) The response of cardiovascular regulatory mechanisms, such as the chemoreflex, adenosine, nitric oxide, and angiotensin II on prenatal hypoxia. (2) The role of the placenta in causing and attenuating the effects of hypoxia. (3) Environmental conditions and the mother's health contribution to the development of prenatal hypoxia. (4) The sex-dependent effects of prenatal hypoxia on cardiovascular regulatory mechanisms and the connection between hypoxia-inducible factors and circadian variability. We identified that the possible relationship between the effects of prenatal hypoxia on the cardiovascular regulatory mechanism may vary depending on circadian variability and phase of the days. In summary, even short-term prenatal hypoxia significantly affects cardiovascular regulatory mechanisms and programs hypertension in adulthood, while prenatal programming effects are not only dependent on the critical period, and sensitivity can change within circadian oscillations.
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