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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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Potential mechanisms underlying fetal hypoxia-induced hypotensive response in female offspring.The ovary releases estrogen and other ovarian hormones/factors. Estrogen down-regulates arterial blood pressure, but other ovarian factors may counteract the effect of estrogen. Antenatal hypoxia leads to programming of a predominating decrease of ovarian progesterone/or other factors release but down-regulation of vascular estrogen effect, overall resulting in development of hypotensive reactivity in female offspring.
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pone-0098743-g008: Potential mechanisms underlying fetal hypoxia-induced hypotensive response in female offspring.The ovary releases estrogen and other ovarian hormones/factors. Estrogen down-regulates arterial blood pressure, but other ovarian factors may counteract the effect of estrogen. Antenatal hypoxia leads to programming of a predominating decrease of ovarian progesterone/or other factors release but down-regulation of vascular estrogen effect, overall resulting in development of hypotensive reactivity in female offspring.

Mentions: The present study demonstrated further that estrogen replacement in OVX animals decreased blood pressure response in normoxic control females. This supports the notion that estrogen plays an important role in regulating arterial blood pressure and in the protection of females from development of hypertensive reactivity. The finding that estrogen replacement in OVX animals had no significant effect on angiotensin II-mediated blood pressure response in antenatal hypoxic animals is very intriguing, and suggests a complexity of mechanisms in hypoxia-induced programming of ovarian steroid hormone function in female offspring. As shown in the diagram of Figure 8, antenatal hypoxia may cause a decreased ovarian progesterone/or other unknown factors release, leading to increased the relative ratio of estrogen to progesterone/other factor and shifted the balance of vasoconstriction/vasodilation, resulting in development of hypotensive reactivity in female offspring. Thus, in sham animals the effect of decreased ovarian steroid hormone other than estrogen release predominates with the phenotypic response of reduced blood pressure, which was abrogated in OVX animals. In OVX animals, the diminished effect of estrogen replacement on blood pressure response in hypoxic animals is likely to attribute to antenatal hypoxia-mediated down-regulation of estrogen-mediated vascular response. Indeed, the previous study of intrauterine growth restriction animal model demonstrated a significant decrease in vascular expression of estrogen receptors in offspring [45].


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)

Potential mechanisms underlying fetal hypoxia-induced hypotensive response in female offspring.The ovary releases estrogen and other ovarian hormones/factors. Estrogen down-regulates arterial blood pressure, but other ovarian factors may counteract the effect of estrogen. Antenatal hypoxia leads to programming of a predominating decrease of ovarian progesterone/or other factors release but down-regulation of vascular estrogen effect, overall resulting in development of hypotensive reactivity in female offspring.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098743-g008: Potential mechanisms underlying fetal hypoxia-induced hypotensive response in female offspring.The ovary releases estrogen and other ovarian hormones/factors. Estrogen down-regulates arterial blood pressure, but other ovarian factors may counteract the effect of estrogen. Antenatal hypoxia leads to programming of a predominating decrease of ovarian progesterone/or other factors release but down-regulation of vascular estrogen effect, overall resulting in development of hypotensive reactivity in female offspring.
Mentions: The present study demonstrated further that estrogen replacement in OVX animals decreased blood pressure response in normoxic control females. This supports the notion that estrogen plays an important role in regulating arterial blood pressure and in the protection of females from development of hypertensive reactivity. The finding that estrogen replacement in OVX animals had no significant effect on angiotensin II-mediated blood pressure response in antenatal hypoxic animals is very intriguing, and suggests a complexity of mechanisms in hypoxia-induced programming of ovarian steroid hormone function in female offspring. As shown in the diagram of Figure 8, antenatal hypoxia may cause a decreased ovarian progesterone/or other unknown factors release, leading to increased the relative ratio of estrogen to progesterone/other factor and shifted the balance of vasoconstriction/vasodilation, resulting in development of hypotensive reactivity in female offspring. Thus, in sham animals the effect of decreased ovarian steroid hormone other than estrogen release predominates with the phenotypic response of reduced blood pressure, which was abrogated in OVX animals. In OVX animals, the diminished effect of estrogen replacement on blood pressure response in hypoxic animals is likely to attribute to antenatal hypoxia-mediated down-regulation of estrogen-mediated vascular response. Indeed, the previous study of intrauterine growth restriction animal model demonstrated a significant decrease in vascular expression of estrogen receptors in offspring [45].

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