Chronic hypoxia in pregnancy affected vascular tone of renal interlobar arteries in the offspring.

Jiaqi Tang,Xiaolin Zhu,Yuan Zhong,Weisheng Li,Zhice Xu,Ningjing Chen,Jiayue Li,Na Li,Caiping Mao,Chonglong Wu,Shuixiu Xia,Qinqin Gao,Zhoufeng Zhu,Dawei Li,Lingjun Li,Qing Tu,Xiang Li,Xiuwen Zhou

doi:10.1038/srep09723

Abstract

Hypoxia during pregnancy could affect development of fetuses as well as cardiovascular systems in the offspring. This study was the first to demonstrate the influence and related mechanisms of prenatal hypoxia (PH) on renal interlobar arteries (RIA) in the 5-month-old male rat offspring. Following chronic hypoxia during pregnancy, phenylephrine induced significantly higher pressor responses and greater vasoconstrictions in the offspring. Nitric oxide mediated vessel relaxation was altered in the RIA. Phenylephrine-stimulated free intracellular calcium was significantly higher in the RIA of the PH group. The activity and expression of L-type calcium channel (Cav1.2), not T-type calcium channel (Cav3.2), was up-regulated. The whole-cell currents of calcium channels and the currents of Cav1.2 were increased compared with the control. In addition, the whole-cell K+ currents were decreased in the offspring exposed to prenatal hypoxia. Activity of large-conductance Ca2+-activated K+ channels and the expression of MaxiKα was decreased in the PH group. The results provide new information regarding the influence of prenatal hypoxia on the development of the renal vascular system, and possible underlying cellular and ion channel mechanisms involved.

Highlights

Hypoxia during pregnancy could affect development of fetuses as well as cardiovascular systems in the offspring
The results provide new information regarding the influence of prenatal hypoxia on the development of the renal vascular system, and possible underlying cellular and ion channel mechanisms involved
The present study found PE-mediated pressor responses and vascular tension of renal interlobar arteries (RIA) were significantly higher in the prenatal hypoxia (PH) group, as new finding of functional changes in blood pressure and renal vascular responses following prenatal exposure to hypoxia

Summary

Introduction

Hypoxia during pregnancy could affect development of fetuses as well as cardiovascular systems in the offspring. The results provide new information regarding the influence of prenatal hypoxia on the development of the renal vascular system, and possible underlying cellular and ion channel mechanisms involved. Both of them can cause structural changes in cells[6,7,8] It is unknown whether autophagy or apoptosis may occur in renal vascular systems following chronic hypoxia during early developmental periods. This study used the prenatal hypoxia (PH) model and determined key molecular elements in the pathways of autophagy and apoptosis in the renal vessels of the offspring exposed to chronic hypoxia during pregnancy. The present study hypothesized that prenatal hypoxia may induce functional and molecular changes in renal blood vessels. There has been very limited information regarding influence and underlying mechanism of prenatal hypoxia-affected ion channel activity in renal vessels. The data gained may provide important information on whether and how chronic hypoxia during early developmental stages affects renal blood vessels

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Discussion

Conclusion