Gestational hypoxia increases reactive oxygen species and inhibits steroid hormone-mediated upregulation of Ca2+-activated K+ channel function in uterine arteries

Hypertension

Volumn 64, Issue 2, 2014, Pages 415-422

  Zhu, Ronghui ^a   Huang, Xiaohui ^a   Hu, Xiang Qun ^a   Xiao, Daliao ^a   Zhang, Lubo ^a  

^a LOMA LINDA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

anoxia; oxidative stress; uterine artery

Indexed keywords

ACETYLCYSTEINE; ESTRADIOL; LARGE CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNEL; PROGESTERONE; REACTIVE OXYGEN METABOLITE; SMALL CONDUCTANCE CALCIUM ACTIVATED POTASSIUM CHANNEL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLOOD VESSEL REACTIVITY; BLOOD VESSEL TONE; CONTROLLED STUDY; DOWN REGULATION; EXPERIMENTAL SHEEP; FEMALE; HYPOXIA; NONHUMAN; OXIDATIVE STRESS; PLACENTA CIRCULATION; PREGNANCY DISORDER; PRENATAL GROWTH; PRIORITY JOURNAL; UPREGULATION; UTERINE ARTERY; UTERUS RELAXATION;

ANOXIA; OXIDATIVE STRESS; UTERINE ARTERY;

ANIMALS; ANOXIA; ESTRADIOL; FEMALE; POTASSIUM CHANNELS, CALCIUM-ACTIVATED; PREGNANCY; PROGESTERONE; REACTIVE OXYGEN SPECIES; SHEEP; UP-REGULATION; UTERINE ARTERY;

EID: 84904513225     PISSN: 0194911X     EISSN: 15244563     Source Type: Journal    
DOI: 10.1161/HYPERTENSIONAHA.114.03555     Document Type: Article

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