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

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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 Ca ²⁺-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.

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Physiological roles and properties of potassium channels in arterial smooth muscle.

M T Nelson, J Quayle (1995)

This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.

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Douglas R. Green (2005)

For more than a decade, it has been apparent that apoptosis and other forms of cell death are often controlled at one or more crucial steps involving the mitochondria. Recent findings, including an elegant investigation in a recent issue of Cell (Hao et al., 2005), have helped to elucidate fundamental aspects of this involvement while raising puzzling new questions about mitochondrial routes to cellular demise. The emerging, if preliminary, perspective these new studies provide may represent either a refinement of our views of how cells die or, perhaps, the beginnings of what amounts to a reformulation of our ideas.

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Developmental Programming of Cardiovascular Dysfunction by Prenatal Hypoxia and Oxidative Stress

Dino Giussani, Emily Camm, Youguo Niu … (2012)

Fetal hypoxia is a common complication of pregnancy. It has been shown to programme cardiac and endothelial dysfunction in the offspring in adult life. However, the mechanisms via which this occurs remain elusive, precluding the identification of potential therapy. Using an integrative approach at the isolated organ, cellular and molecular levels, we tested the hypothesis that oxidative stress in the fetal heart and vasculature underlies the molecular basis via which prenatal hypoxia programmes cardiovascular dysfunction in later life. In a longitudinal study, the effects of maternal treatment of hypoxic (13% O2) pregnancy with an antioxidant on the cardiovascular system of the offspring at the end of gestation and at adulthood were studied. On day 6 of pregnancy, rats (n = 20 per group) were exposed to normoxia or hypoxia ± vitamin C. At gestational day 20, tissues were collected from 1 male fetus per litter per group (n = 10). The remaining 10 litters per group were allowed to deliver. At 4 months, tissues from 1 male adult offspring per litter per group were either perfusion fixed, frozen, or dissected for isolated organ preparations. In the fetus, hypoxic pregnancy promoted aortic thickening with enhanced nitrotyrosine staining and an increase in cardiac HSP70 expression. By adulthood, offspring of hypoxic pregnancy had markedly impaired NO-dependent relaxation in femoral resistance arteries, and increased myocardial contractility with sympathetic dominance. Maternal vitamin C prevented these effects in fetal and adult offspring of hypoxic pregnancy. The data offer insight to mechanism and thereby possible targets for intervention against developmental origins of cardiac and peripheral vascular dysfunction in offspring of risky pregnancy.

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Journal

Journal ID (nlm-ta): Sci Rep

Journal ID (iso-abbrev): Sci Rep

Title: Scientific Reports

Publisher: Nature Publishing Group

ISSN (Electronic): 2045-2322

Publication date (Electronic): 18 May 2015

Publication date Collection: 2015

Volume: 5

Electronic Location Identifier: 9723

Affiliations

[1 ]Institute for Fetology, First Hospital of Soochow University , Suzhou, China

[2 ]Center for Perinatal Biology, Loma Linda University , California, USA

Author notes

[a ] xuzhice@ 123456suda.edu.cn

[*]

These authors contributed equally to this work.

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Publisher Item ID: srep09723

DOI: 10.1038/srep09723

PMC ID: 4434890

PubMed ID: 25983078

SO-VID: 9e2f6ede-d306-4b30-a309-34d445656d35

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

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Most cited references 29

Physiological roles and properties of potassium channels in arterial smooth muscle.

Apoptotic pathways: ten minutes to dead.

Developmental Programming of Cardiovascular Dysfunction by Prenatal Hypoxia and Oxidative Stress

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