Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in female offspring.

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

Effect of antenatal hypoxia on the baroreflex sensitivity in female offspring.

<p>Heart rate and mean arterial blood pressure (MAP) responses to angiotensin II (300 ng/kg; 1 ml/kg, <i>i.v.</i>) were measured in 3-month-old female offspring that had been exposed <i>in utero</i> to normoxia or hypoxia. The baroreflex sensitivity was determined as the slope of heart rate/MAP (bpm/mmHg). Data are means ± SEM, n = 9.</p

Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in male offspring.

<p>Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, <i>i.v.</i>) were measured in 3-month-old male offspring that had been exposed <i>in utero</i> to normoxia or hypoxia. Data are means ± SEM, n = 7. * P<0.05, hypoxia <i>vs.</i> normoxia.</p

Potential mechanisms underlying fetal hypoxia-induced hypotensive response in female offspring.

<p>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.</p

Effect of antenatal hypoxia on baseline and Angiotensin II-induced maximal mean arterial blood pressure responses in adult offspring.

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

Effect of antenatal hypoxia on angiotensin II-induced blood pressure response in male offspring.

<p>Systolic (SBP), diastolic (DBP), and mean (MAP) arterial blood pressure responses to angiotensin II (300 ng/kg; 1 ml/kg, <i>i.v.</i>) were measured in 3-month-old male offspring that had been exposed <i>in utero</i> to normoxia or hypoxia. Data are means ± SEM, n = 7. * P<0.05, hypoxia <i>vs.</i> normoxia.</p

Effect of Hypoxia on Body Weight and Basal Heart Rate.

<p>Note: BW, body weight; HR, heart rate; *P < 0.05, Hypoxia (H) vs. control(C);</p>a<p>P<0.05, vs. sham; ^bP<0.05, vs. OVX.</p

Effect of antenatal hypoxia on angiotensin II-induced arterial contractions in female offspring.

<p>Angiotensin II (Ang II)-induced contractions were determined in isolated aortas of adult female offspring that had been exposed <i>in utero</i> to normoxia or hypoxia. Data are means ± SEM, n = 9-10. The values of pD₂ and the maximal response were presented in the text.</p

Effect of nicotine on CpG methylation of AT_1aR promoter in aortic rings in male offspring.

<p>Aortic rings were freshly isolated from male adult offspring that had been exposed in utero to saline control or nicotine. DNA was isolated and methylation levels were determined by methylation-specific real-time PCR. Data are means ± SEM of tissues from saline control (n = 4) and nicotine (n = 4). The sample sizes represent the animal number from different litters of each group. Data were analyzed by student <i>t</i>-test. ^*P <0.05 vs. control.</p

Effect of nicotine on Ang II-induced contractions and Ca²⁺ mobilization in mesenteric arteries in adult offspring.

<p>Ang II-induced contractions of pressurized mesenteric arteries were determined in male adult offspring that had been exposed in utero to saline control or nicotine. <b>A</b>, Typical recordings of Ang II (100 nM)-induced decreases in the arterial diameter and increments in [Ca²⁺]_i in the same tissue from saline control and nicotine-treated groups. Ang II-induced contractions (<b>B</b>), [Ca²⁺]_i (<b>C</b>), and arterial diameter change/[Ca²⁺]_i ratio (<b>D</b>) in mesenteric arteries from the control and nicotine-treated animals. Data are means ± SEM of tissues from saline control (n = 7) and nicotine (n = 8). The sample sizes represent the animal number from different litters of each group. Data were analyzed by student <i>t</i>-test. ^*P <0.05 vs. control.</p