Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity

Maternal obesity increases the risk of preterm delivery and rapid transition of offspring from a hypoxemic environment to a normal or elevated oxygen environment, especially if the baby receives oxygen therapy. Maternal obesity may also increase offspring risk of developing hypertension. Thus, we examined whether neonatal hyperoxia (HO) leads to elevated blood pressure (BP) in offspring from lean mothers and exacerbates adverse impact of maternal obesity on offspring BP regulation. Male and female Sprague-Dawley offspring from lean and high-fat diet-fed obese mothers (<i>n</i> = 12-18 mothers/group) were exposed to room air (∼21% O<sub>2</sub>) or HO (80% O<sub>2</sub>) between <i>postnatal days</i> P3 and P10 and then returned to room air. At 12 wk of age, offspring were instrumented with telemetry probes to measure BP and heart rate (HR). Contrary to our hypothesis, neonatal HO was associated with lower BP compared with control offspring from lean mothers (males: 105 ± 1 vs. 111 ± 1 mmHg; females: 102 ± 0.4 vs. 108 ± 0.4 mmHg) and also reduced BP and HR in hypertensive obese offspring from obese mothers (males: 117 ± 1 vs. 123 ± 1 mmHg and 351 ± 4 vs. 358 ± 5 beats/min; females: 113 ± 1 vs. 116 ± 1 mmHg and 376 ± 2 vs. 390 ± 4 beats/min). In lean offspring from lean mothers, neonatal HO was associated with reduced +dP/d<i>t</i><sub>max</sub>, whereas in obese offspring from obese mothers, HO attenuated cardiac dysfunction when compared with obese offspring not submitted to HO. These results suggest that exposure to HO in early postnatal life is not associated with elevated BP in early adulthood and it does not exacerbate the hypertensive effects of maternal obesity on offspring BP regulation.<b>NEW & NOTEWORTHY</b> Maternal obesity increases risk for preterm birth and neonatal oxygen exposure. We tested whether hyperoxia (80% O<sub>2</sub>, P3-P10) worsens maternal obesity-induced hypertension. At 14 wk, BP measured by telemetry showed that hyperoxia unexpectedly lowered BP in lean and obese offspring and attenuated cardiac dysfunction in obese offspring. These findings indicate that neonatal hyperoxia does not exacerbate maternal obesity-induced hypertension and may mitigate early cardiac dysfunction.

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Journal
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Published
2025-11-21
DOI
https://doi.org/10.1152/ajpregu.00221.2025
Primary Topic
Gestational Diabetes Research and Management
Type
article
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article

Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity

John E. Hall, Jussara M. do Carmo, Alan J. Mouton, Xuemei Dai et al.
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Gestational Diabetes Research and Management
article

Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity

John E. Hall, Jussara M. do Carmo, Alan J. Mouton, Xuemei Dai, Emily C. Ladnier, Zhen Wang, Alexandre A. da Silva
article en

Abstract

Maternal obesity increases the risk of preterm delivery and rapid transition of offspring from a hypoxemic environment to a normal or elevated oxygen environment, especially if the baby receives oxygen therapy. Maternal obesity may also increase offspring risk of developing hypertension. Thus, we examined whether neonatal hyperoxia (HO) leads to elevated blood pressure (BP) in offspring from lean mothers and exacerbates adverse impact of maternal obesity on offspring BP regulation. Male and female Sprague-Dawley offspring from lean and high-fat diet-fed obese mothers (<i>n</i> = 12-18 mothers/group) were exposed to room air (∼21% O<sub>2</sub>) or HO (80% O<sub>2</sub>) between <i>postnatal days</i> P3 and P10 and then returned to room air. At 12 wk of age, offspring were instrumented with telemetry probes to measure BP and heart rate (HR). Contrary to our hypothesis, neonatal HO was associated with lower BP compared with control offspring from lean mothers (males: 105 ± 1 vs. 111 ± 1 mmHg; females: 102 ± 0.4 vs. 108 ± 0.4 mmHg) and also reduced BP and HR in hypertensive obese offspring from obese mothers (males: 117 ± 1 vs. 123 ± 1 mmHg and 351 ± 4 vs. 358 ± 5 beats/min; females: 113 ± 1 vs. 116 ± 1 mmHg and 376 ± 2 vs. 390 ± 4 beats/min). In lean offspring from lean mothers, neonatal HO was associated with reduced +dP/d<i>t</i><sub>max</sub>, whereas in obese offspring from obese mothers, HO attenuated cardiac dysfunction when compared with obese offspring not submitted to HO. These results suggest that exposure to HO in early postnatal life is not associated with elevated BP in early adulthood and it does not exacerbate the hypertensive effects of maternal obesity on offspring BP regulation.<b>NEW & NOTEWORTHY</b> Maternal obesity increases risk for preterm birth and neonatal oxygen exposure. We tested whether hyperoxia (80% O<sub>2</sub>, P3-P10) worsens maternal obesity-induced hypertension. At 14 wk, BP measured by telemetry showed that hyperoxia unexpectedly lowered BP in lean and obese offspring and attenuated cardiac dysfunction in obese offspring. These findings indicate that neonatal hyperoxia does not exacerbate maternal obesity-induced hypertension and may mitigate early cardiac dysfunction.

American Journal of Physiology-Regulatory, Integrative and Comparative PhysiologyVol. 330(1)
University of Mississippi Medical Center (US)
Openalex Percentile: Top 54%
Gestational Diabetes Research and Management
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