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Antenatal hypoxia induces programming of reduced arterial blood pressure response in female rat offspring: role of ovarian function.

Xiao D, Huang X, Xue Q, Zhang L - PLoS ONE (2014)

Bottom Line: The baroreflex sensitivity was not significantly altered.Consistent with the reduced blood pressure response, antenatal hypoxia significantly decreased Ang II-induced arterial vasoconstriction in female offspring.Hypoxia-mediated ovary dysfunction results in the phenotype of reduced vascular contractility and BP response in female adult offspring.

View Article: PubMed Central - PubMed

Affiliation: Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.

ABSTRACT
In utero exposure to adverse environmental factors increases the risk of cardiovascular disease in adulthood. The present study tested the hypothesis that antenatal hypoxia causes a gender-dependent programming of altered arterial blood pressure response (BP) in adult offspring. Time-dated pregnant rats were divided into normoxic and hypoxic (10.5% O2 from days 15 to 21 of gestation) groups. The experiments were conducted in adult offspring. Antenatal hypoxia caused intrauterine growth restriction, and resulted in a gender-dependent increase Angiotensin II (Ang II)-induced BP response in male offspring, but significant decrease in BP response in female offspring. The baroreflex sensitivity was not significantly altered. Consistent with the reduced blood pressure response, antenatal hypoxia significantly decreased Ang II-induced arterial vasoconstriction in female offspring. Ovariectomy had no significant effect in control animals, but significantly increased Ang II-induced maximal BP response in prenatally hypoxic animals and eliminated the difference of BP response between the two groups. Estrogen replacement in ovariectomized animals significantly decreased the BP response to angiotensin II I only in control, but not in hypoxic animals. The result suggests complex programming mechanisms of antenatal hypoxia in regulation of ovary function. Hypoxia-mediated ovary dysfunction results in the phenotype of reduced vascular contractility and BP response in female adult offspring.

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Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in female offspring.Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were measured in 3-month-old female offspring that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 9. * P<0.05, hypoxia vs. normoxia.
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pone-0098743-g002: Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in female offspring.Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were measured in 3-month-old female offspring that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 9. * P<0.05, hypoxia vs. normoxia.

Mentions: Ang II produced a time-dependent increase in arterial blood pressure in both control and hypoxia-treated adult offspring. As shown in Figure 1, antenatal hypoxia significantly enhanced Ang II-stimulated systolic, diastolic and mean arterial blood pressure in male offspring, as compared with the normoxic control group. However, hypoxia significantly reduced Ang II-stimulated systolic, diastolic and mean arterial blood pressure in female offspring (Figure 2). The baroreflex sensitivity determined as the slope of heart rate/mean arterial pressure was not significantly different between control and hypoxic groups in female offspring (Figure 3). Consistent with the reduced blood pressure response in female offspring, Ang II-induced arterial contractions were also significantly decreased in hypoxic animals (Figure 4). In isolated aortas, KCl (120 mmol/L)-induced contractions were not significantly different between hypoxic and normoxic control groups (2.03±0.11 vs. 1.98±0.11 g; P>0.05) (data not shown), suggesting the lack of effect of antenatal hypoxia on electromechanic coupling and vascular contractility. As shown in Figure 4, antenatal hypoxia had no significant effect on the pD2 (–log EC50) values of angiotensin II-induced contractions, as compared with the control (7.9±0.3 vs. 7.7±0.2, P>0.05). However, angiotensin II-induced maximal contractions were significantly decreased in antenatal hypoxia-treated female offspring, as compared with the control group (32.7±3.0% vs. 12.6±1.4% of KCl responses, P<0.05).


Antenatal hypoxia induces programming of reduced arterial blood pressure response in female rat offspring: role of ovarian function.

Xiao D, Huang X, Xue Q, Zhang L - PLoS ONE (2014)

Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in female offspring.Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were measured in 3-month-old female offspring that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 9. * P<0.05, hypoxia vs. normoxia.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4048263&req=5

pone-0098743-g002: Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in female offspring.Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were measured in 3-month-old female offspring that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 9. * P<0.05, hypoxia vs. normoxia.
Mentions: Ang II produced a time-dependent increase in arterial blood pressure in both control and hypoxia-treated adult offspring. As shown in Figure 1, antenatal hypoxia significantly enhanced Ang II-stimulated systolic, diastolic and mean arterial blood pressure in male offspring, as compared with the normoxic control group. However, hypoxia significantly reduced Ang II-stimulated systolic, diastolic and mean arterial blood pressure in female offspring (Figure 2). The baroreflex sensitivity determined as the slope of heart rate/mean arterial pressure was not significantly different between control and hypoxic groups in female offspring (Figure 3). Consistent with the reduced blood pressure response in female offspring, Ang II-induced arterial contractions were also significantly decreased in hypoxic animals (Figure 4). In isolated aortas, KCl (120 mmol/L)-induced contractions were not significantly different between hypoxic and normoxic control groups (2.03±0.11 vs. 1.98±0.11 g; P>0.05) (data not shown), suggesting the lack of effect of antenatal hypoxia on electromechanic coupling and vascular contractility. As shown in Figure 4, antenatal hypoxia had no significant effect on the pD2 (–log EC50) values of angiotensin II-induced contractions, as compared with the control (7.9±0.3 vs. 7.7±0.2, P>0.05). However, angiotensin II-induced maximal contractions were significantly decreased in antenatal hypoxia-treated female offspring, as compared with the control group (32.7±3.0% vs. 12.6±1.4% of KCl responses, P<0.05).

Bottom Line: The baroreflex sensitivity was not significantly altered.Consistent with the reduced blood pressure response, antenatal hypoxia significantly decreased Ang II-induced arterial vasoconstriction in female offspring.Hypoxia-mediated ovary dysfunction results in the phenotype of reduced vascular contractility and BP response in female adult offspring.

View Article: PubMed Central - PubMed

Affiliation: Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.

ABSTRACT
In utero exposure to adverse environmental factors increases the risk of cardiovascular disease in adulthood. The present study tested the hypothesis that antenatal hypoxia causes a gender-dependent programming of altered arterial blood pressure response (BP) in adult offspring. Time-dated pregnant rats were divided into normoxic and hypoxic (10.5% O2 from days 15 to 21 of gestation) groups. The experiments were conducted in adult offspring. Antenatal hypoxia caused intrauterine growth restriction, and resulted in a gender-dependent increase Angiotensin II (Ang II)-induced BP response in male offspring, but significant decrease in BP response in female offspring. The baroreflex sensitivity was not significantly altered. Consistent with the reduced blood pressure response, antenatal hypoxia significantly decreased Ang II-induced arterial vasoconstriction in female offspring. Ovariectomy had no significant effect in control animals, but significantly increased Ang II-induced maximal BP response in prenatally hypoxic animals and eliminated the difference of BP response between the two groups. Estrogen replacement in ovariectomized animals significantly decreased the BP response to angiotensin II I only in control, but not in hypoxic animals. The result suggests complex programming mechanisms of antenatal hypoxia in regulation of ovary function. Hypoxia-mediated ovary dysfunction results in the phenotype of reduced vascular contractility and BP response in female adult offspring.

Show MeSH
Related in: MedlinePlus