Hypophosphatemia-mediated hypotension in transgenic mice overexpressing human FGF-23

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 297, Issue 4, 2009, Pages

  Liu, Peidang ^a,b   Bai, Xiuying ^c   Wang, Heming ^a   Karaplis, Andrew ^c   Goltzman, David ^c   Miao, Dengshun ^a  

^a NANJING MEDICAL UNIVERSITY   (China)

^b SOUTHEAST UNIVERSITY   (China)

^c MCGILL UNIVERSITY   (Canada)

Author keywords

Blood pressure; Cardiovascular system; Fibroblast growth factor 23; Phosphaturic factor

Indexed keywords

CATECHOLAMINE; FIBROBLAST GROWTH FACTOR 23; PHOSPHATE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLOOD VESSEL REACTIVITY; CARDIOVASCULAR SYSTEM; CONTROLLED STUDY; DISEASE COURSE; DOWN REGULATION; FLUID INTAKE; GENE OVEREXPRESSION; HEART LEFT VENTRICLE; HEART VENTRICLE HYPERTROPHY; HEREDITY; HUMAN; HYPOPHOSPHATEMIA; HYPOTENSION; MOUSE; NONHUMAN; PRIORITY JOURNAL; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; UPREGULATION;

ANIMALS; BLOOD PRESSURE; CATECHOLAMINES; DIET; DOSE-RESPONSE RELATIONSHIP, DRUG; FEMALE; FIBROBLAST GROWTH FACTORS; HUMANS; HYPERTROPHY, LEFT VENTRICULAR; HYPOPHOSPHATEMIA; HYPOTENSION; MALE; MICE; MICE, TRANSGENIC; PHENOTYPE; PHOSPHATES; RECEPTOR, ANGIOTENSIN, TYPE 1; RECEPTORS, ADRENERGIC, ALPHA-1; RECEPTORS, FIBROBLAST GROWTH FACTOR; RENIN-ANGIOTENSIN SYSTEM; RNA, MESSENGER; UP-REGULATION; VASOCONSTRICTION; VASOCONSTRICTOR AGENTS; VENTRICULAR FUNCTION, LEFT;

EID: 70349627689     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00581.2009     Document Type: Article

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