Related Experiment Video
Updated: Jan 6, 2026

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
Published on: October 19, 2013
Neonatal hyperoxia exposure does not exacerbate hypertension programmed by maternal obesity
Jussara M do Carmo1, John E Hall1, Xuemei Dai1
1Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiorenal and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, Mississippi, United States.
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 (n = 12-18 mothers/group) were exposed to room air (∼21% O2) or HO (80% O2) between postnatal days 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/dtmax, 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.NEW & NOTEWORTHY Maternal obesity increases risk for preterm birth and neonatal oxygen exposure. We tested whether hyperoxia (80% O2, 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.
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 (n = 12-18 mothers/group) were exposed to room air (∼21% O2) or HO (80% O2) between postnatal days 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/dtmax, 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.NEW & NOTEWORTHY Maternal obesity increases risk for preterm birth and neonatal oxygen exposure. We tested whether hyperoxia (80% O2, 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.
Related Concept Videos
Hypertension II: Pathophysiology
Hypertension and Regulation of Blood Pressure
Hormonal Regulation
Hypertension I: Introduction
Pharmacokinetics in Obese Patients: Drug Metabolism and Excretion
Hypertension V: Nursing Management

