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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 baseline and Angiotensin II-induced maximal mean arterial blood pressure responses in adult offspring.The baseline and maximal mean arterial blood pressure (MAP) responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were determined in adult male, sham, ovariectomy (OVX), and OVX plus estrogen (E2) replacement female offspring that had been exposed in utero to normoxia (control) or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. control; † P<0.05, OVX vs. sham; # P<0.05, OVX+E2vs. OVX.
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pone-0098743-g007: Effect of antenatal hypoxia on baseline and Angiotensin II-induced maximal mean arterial blood pressure responses in adult offspring.The baseline and maximal mean arterial blood pressure (MAP) responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were determined in adult male, sham, ovariectomy (OVX), and OVX plus estrogen (E2) replacement female offspring that had been exposed in utero to normoxia (control) or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. control; † P<0.05, OVX vs. sham; # P<0.05, OVX+E2vs. OVX.

Mentions: To further determine the role of estrogen in antenatal hypoxia-mediated blood pressure response, Ang II-induced blood pressure response was measured in OVX animals with estrogen replacement. In contrast to the findings in the sham animals, Ang II-induced blood pressure response was significantly greater in hypoxic than in control groups in OVX animals with estrogen replacement (Figure 6 right panel). In male offspring, the basal heart rate (Table 1) and mean arterial blood pressure (Figure 7) was not significantly different between control and hypoxic offspring. Similarly, in female offspring hypoxia also did not alter basal heart rate and mean arterial blood pressure. As shown in Figure 7, OVX had no significant effect on Ang II-induced blood pressure response in normoxic OVX as compared with normoxic intact animals, but significantly increased it in hypoxic OVX as compared with hypoxic intact animals and eliminated the difference between the control and antenatal hypoxic female offspring seen in the sham animals. Compared with OVX animals, estrogen replacement caused a significant decrease in angiotensin II-mediated response in normoxic control animals, but not in antenatal hypoxic animals, resulting in a reversal of blood pressure responses seen in the sham animals.


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 baseline and Angiotensin II-induced maximal mean arterial blood pressure responses in adult offspring.The baseline and maximal mean arterial blood pressure (MAP) responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were determined in adult male, sham, ovariectomy (OVX), and OVX plus estrogen (E2) replacement female offspring that had been exposed in utero to normoxia (control) or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. control; † P<0.05, OVX vs. sham; # P<0.05, OVX+E2vs. OVX.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098743-g007: Effect of antenatal hypoxia on baseline and Angiotensin II-induced maximal mean arterial blood pressure responses in adult offspring.The baseline and maximal mean arterial blood pressure (MAP) responses to angiotensin II (300 ng/kg; 1 ml/kg, i.v.) were determined in adult male, sham, ovariectomy (OVX), and OVX plus estrogen (E2) replacement female offspring that had been exposed in utero to normoxia (control) or hypoxia. Data are means ± SEM, n = 7–9. * P<0.05, hypoxia vs. control; † P<0.05, OVX vs. sham; # P<0.05, OVX+E2vs. OVX.
Mentions: To further determine the role of estrogen in antenatal hypoxia-mediated blood pressure response, Ang II-induced blood pressure response was measured in OVX animals with estrogen replacement. In contrast to the findings in the sham animals, Ang II-induced blood pressure response was significantly greater in hypoxic than in control groups in OVX animals with estrogen replacement (Figure 6 right panel). In male offspring, the basal heart rate (Table 1) and mean arterial blood pressure (Figure 7) was not significantly different between control and hypoxic offspring. Similarly, in female offspring hypoxia also did not alter basal heart rate and mean arterial blood pressure. As shown in Figure 7, OVX had no significant effect on Ang II-induced blood pressure response in normoxic OVX as compared with normoxic intact animals, but significantly increased it in hypoxic OVX as compared with hypoxic intact animals and eliminated the difference between the control and antenatal hypoxic female offspring seen in the sham animals. Compared with OVX animals, estrogen replacement caused a significant decrease in angiotensin II-mediated response in normoxic control animals, but not in antenatal hypoxic animals, resulting in a reversal of blood pressure responses seen in the sham animals.

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