Prenatal Hypoxia Induced Dysfunction in Cerebral Arteries of Offspring Rats

Figures

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  Figure 1. Angiotensin II (AII)‐induced contraction and endothelial nitric oxide synthase (eNOS)‐related relaxation in the offspring middle cerebral arteries (MCA). A, Cumulative concentration of AII induced response curves in MCA. Potassium chloride (KCl) mediated constriction in both groups. B through D, showed dose–response curves of AII‐induced contraction with or without L‐Name (NG‐nitro‐l‐arginine), losartan, and PD123,319, respectively. *P<0.05, **P<0.01, ***P<0.001, # P<0.05, control vs PH. N=10, n=10 to 12 in each group. C indicates control; PH, prenatal‐hypoxia group.

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  Figure 2. Membrane voltage‐dependent calcium channels of middle cerebral arteries. A, Cumulative angiotensin II (AII)‐mediated response curves in the presence or absence of nifedipine. B, The comparison of cumulative AII‐mediated response curves in the presence of nifedipine and mibefradil between C and PH groups. N=12, n=12 to 14 in each group, **P<0.01, ***P<0.001. # P<0.05, control vs PH. C indicates control; PH, prenatal‐hypoxia group.

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  Figure 3. Whole‐cell calcium channel currents in vascular smooth muscle cells. The first real‐time images represented the whole‐cell calcium channel currents of both groups. A, Whole‐cell calcium current density, activation, and inactivation curves at depolarizing voltage steps. B and C, AII potentiated the amplitude of calcium current density in the control but not in the PH group. Meanwhile, the activation and inactivation curves were not affected by AII. N=6, n=6, 2 to 4 cells for each offspring, *P<0.05, **P<0.01, ***P<0.001. AII indicates angiotensin II; C, control; PH, prenatal‐hypoxia group.

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  Figure 4. Receptor‐gated calcium channels and sarcoendoplasmic reticulum Ca2+‐ATPase. A through C, AII‐induced contractions in the presence or absence of 2APB (2‐aminoethyl diphenylborinate, 10−7 mol/L and 10−5 mol/L), ryanodine, and thapsigargin in both groups. D, Caffeine caused contraction of middle cerebral arteries and calcium transient of vascular smooth muscle cells in both groups. The insets show the real‐time curves of caffeine‐induced calcium transients. N=7, n=7 to 13 in each group, *P<0.05, **P<0.01, ***P<0.001. # P<0.05, control vs PH. AII indicates angiotensin II; C, control; PH, prenatal‐hypoxia group.

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  Figure 5. Relative mRNA expression in the cerebral arteries. A, The mRNA expression of angiotensin II receptors, (B) expression of voltage‐dependent calcium channel isoforms, and (C) sarcoplasmic reticulum receptors and Ca2+‐ATPase expression. In the prenatal‐hypoxia group, AT1A, AT1B, AT2R, Cav1.2α1C, Cav3.2α1H, and RyR2 were increased compared with the control; Cavβ2, Cavβ3, Ip3r1‐3, and Serca1/2 showed no significant differences between the groups. N=4, *P<0.05, **P<0.01, ***P<0.001. C indicates control group.

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  Figure 6. This image shows how prenatal hypoxia affects vascular functions in the middle cerebral arteries (MCA), which may lead to increased risks of stroke. AT1R, AT2R indicate AT1 and 2 receptors; Cav1.2, L‐type calcium channels; eNOS, endothelial nitric oxide synthase; IP3r, IP 3 receptor; PKC, protein kinase C; PLC, phospholipase C; RyR, ryanodine receptor; Serca, sarcoendoplasmic reticulum Ca2+‐ATPase.