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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 ovariectomy and estrogen replacement 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 OVX female offspring (Left panel) and in OVX + E2 replacement (Right panel) that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. normoxia.
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pone-0098743-g006: Effect of ovariectomy and estrogen replacement 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 OVX female offspring (Left panel) and in OVX + E2 replacement (Right panel) that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. normoxia.

Mentions: To determine whether ovarian function plays a key role in the antenatal hypoxia-induced effect in female offspring, Ang II-induced blood pressure response was determined in OVX animals. Unlike the findings in the sham animals, in OVX animals there was no significant difference in Ang II-induced blood pressure response between the control and hypoxic groups (Figure 6 left panel).


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 ovariectomy and estrogen replacement 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 OVX female offspring (Left panel) and in OVX + E2 replacement (Right panel) that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. normoxia.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098743-g006: Effect of ovariectomy and estrogen replacement 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 OVX female offspring (Left panel) and in OVX + E2 replacement (Right panel) that had been exposed in utero to normoxia or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. normoxia.
Mentions: To determine whether ovarian function plays a key role in the antenatal hypoxia-induced effect in female offspring, Ang II-induced blood pressure response was determined in OVX animals. Unlike the findings in the sham animals, in OVX animals there was no significant difference in Ang II-induced blood pressure response between the control and hypoxic groups (Figure 6 left panel).

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