Limits...
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.

Show MeSH

Related in: MedlinePlus

Effect of antenatal hypoxia on plasma estrogen level in female offspring.Blood plasma was collected from the both control and hypoxia-treated female offspring of sham, OVX and estrogen replacement groups. Plasma estrogen levels were determined with a commercially available Estradiol ELISA kit. Data are means ± SEM, n = 10–14 each group. * P<0.05, OVX vs. sham group.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4048263&req=5

pone-0098743-g005: Effect of antenatal hypoxia on plasma estrogen level in female offspring.Blood plasma was collected from the both control and hypoxia-treated female offspring of sham, OVX and estrogen replacement groups. Plasma estrogen levels were determined with a commercially available Estradiol ELISA kit. Data are means ± SEM, n = 10–14 each group. * P<0.05, OVX vs. sham group.

Mentions: Since our functional data indicated a gender difference in response to antenatal hypoxia, we hypothesized that alteration of estrogen level may play a key role in hypoxia-mediated changes of blood pressure response. We determined the plasma estrogen levels in different groups of female offspring. As shown in figure 5, antenatal hypoxia did not significantly changes plasma estrogen levels, as compared with the control of female offspring in sham, OVX and estrogen-replacement groups. OVX treatment significantly decreased plasma estrogen level, which was restored by estrogen-replacement in both control and hypoxic groups.


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 plasma estrogen level in female offspring.Blood plasma was collected from the both control and hypoxia-treated female offspring of sham, OVX and estrogen replacement groups. Plasma estrogen levels were determined with a commercially available Estradiol ELISA kit. Data are means ± SEM, n = 10–14 each group. * P<0.05, OVX vs. sham group.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098743-g005: Effect of antenatal hypoxia on plasma estrogen level in female offspring.Blood plasma was collected from the both control and hypoxia-treated female offspring of sham, OVX and estrogen replacement groups. Plasma estrogen levels were determined with a commercially available Estradiol ELISA kit. Data are means ± SEM, n = 10–14 each group. * P<0.05, OVX vs. sham group.
Mentions: Since our functional data indicated a gender difference in response to antenatal hypoxia, we hypothesized that alteration of estrogen level may play a key role in hypoxia-mediated changes of blood pressure response. We determined the plasma estrogen levels in different groups of female offspring. As shown in figure 5, antenatal hypoxia did not significantly changes plasma estrogen levels, as compared with the control of female offspring in sham, OVX and estrogen-replacement groups. OVX treatment significantly decreased plasma estrogen level, which was restored by estrogen-replacement in both control and hypoxic groups.

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