Overexpression of the SK3 channel alters vascular remodeling during pregnancy, leading to fetal demise

American Journal of Physiology - Endocrinology and Metabolism

Volumn 303, Issue 7, 2012, Pages

  Rada, Cara C ^a,b   Pierce, Stephanie L ^b   Nuno, Daniel W ^b   Zimmerman, Kathy ^b   Lamping, Kathryn G ^b,c   Bowdler, Noelle C ^b   Weiss, Robert M ^b   England, Sarah K ^a,b  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF IOWA   (United States)

^c VETERANS AFFAIRS MEDICAL CENTER   (United States)

Author keywords

Pregnancy; Small conductance Ca2+activated K+ channel subtype 3; Vasculature

Indexed keywords

CALCIUM ACTIVATED POTASSIUM CHANNEL; SK3 CHANNEL; UNCLASSIFIED DRUG;

ARTICLE; CARDIOVASCULAR PARAMETERS; CONTROLLED STUDY; DEPOLARIZATION; ECHOGRAPHY; FEMALE; FETUS OUTCOME; FETUS WASTAGE; GENE OVEREXPRESSION; HEART EJECTION FRACTION; HEART RATE; INTRAUTERINE GROWTH RETARDATION; MOUSE; NONHUMAN; PHENOTYPE; PREGNANCY; PRIORITY JOURNAL; THICKNESS; TRANSGENIC MOUSE; UTERINE ARTERY; VASCULAR REMODELING; WILD TYPE;

ANIMALS; FEMALE; FETAL DEATH; FETAL GROWTH RETARDATION; HEART RATE; MALE; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; ORGAN SIZE; PLACENTA; PREGNANCY; SMALL-CONDUCTANCE CALCIUM-ACTIVATED POTASSIUM CHANNELS; STROKE VOLUME; ULTRASONOGRAPHY, PRENATAL; UTERINE ARTERY; UTERUS;

EID: 84867167314     PISSN: 01931849     EISSN: 15221555     Source Type: Journal    
DOI: 10.1152/ajpendo.00165.2012     Document Type: Article

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