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.

Highlights

  • The cardiovascular system is a dynamic system that can adapt to adverse conditions to maintain and satisfy homeostasis in the organism

  • We further describe the effects of prenatal hypoxia on cardiovascular regulatory mechanisms: the chemoreflex, adenosine, nitric oxide (NO), reactive oxygen species (ROS), and reninangiotensin-aldosterone system (RAAS), as well as the effects of prenatal hypoxia on morphological-functional changes in the heart, blood vessels, and kidneys (Table 2)

  • Prenatal hypoxia (12 h, embryonic day (ED) 20) during the light phase did not change the circadian rhythms of blood pressure and heart rate in male offspring, as well as the response of the cardiovascular system to vasoconstriction drugs [30,132]; these animals had an altered response to artificial light at night [132], which is considered as a risk factor for the disruption of circadian control and the development of cardiovascular diseases [225]

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Summary

Introduction

The cardiovascular system is a dynamic system that can adapt to adverse conditions to maintain and satisfy homeostasis in the organism. Moderate effects on the foetus include high or low food availability, oxygen deficiency (hypoxia), maternal obesity, inadequate prenatal care, maternal stress, and maternal chronic diseases The consequences of these factors can be identified during pregnancy screening and immediately after birth because they are often associated with a reduction in birth weight and asymmetric organ growth [6]. Prenatal insults do not necessarily have to be manifested by low birth weight (Table 1) and still can lead to the programming of diseases in adulthood This phenomenon is observed after exposure to prenatal hypoxia, which is a common complication in gravidity. 12, 24, 48, h immediately prior to delivery at term 5–19 ED 5–20 ED 15–20 ED from ED–NA 5–20 ED

11–17.5 ED last 15 days of gravidity
Foetus
Reflex Response
Adenosine
Nitric Oxide, A Reactive Oxygen Species
Renin-Angiotensin-Aldosterone System
Morphological-Functional Changes in the Heart and Blood Vessels
Placenta
Mother
Factors Affecting the Consequences of Hypoxia
Circadian Variability
Hypoxia-Inducible Factors
Consequences
Findings
Conclusions
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