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Elevation of extracellular NaCl increases secretion of von Willebrand Factor from endothelial cells
Author(s) -
Dmitrieva Natalia I.,
Burg Maurice B.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.686.3
Subject(s) - von willebrand factor , medicine , endocrinology , hypernatremia , kidney , umbilical vein , vasopressin , renal medulla , platelet , chemistry , sodium , biochemistry , organic chemistry , in vitro
Osmoregulation maintains normal systemic osmolality at 270–290 mosmol/kg. However, it is higher in some organs: 330–335 in spleen, liver and thymus, 400–550 in intervertebral discs, 400 in synovial fluid, and up to 1700 in human renal medulla, where it powers concentration of the urine. During pathological hypernatremia, serum osmolality can rise to 340. Hypernatremia is a known risk factor for thrombosis. Von Willebrand factor (vWF) plays a key role in thrombosis by mediating platelet adhesion to vascular walls. We now find that, in tissue culture of Human Umbilical Vein Endothelia Cells, elevating medium osmolality to 320–380 mosmol/kg by adding NaCl reversibly increases both vWF mRNA and the rate of vWF secretion. In mice, vWF is higher in endothelial cells of the kidney medulla, where NaCl is high, than in kidney cortex, where it is not, as measured by immunostaining. Further, water restriction increases blood vWF. High blood vWF is a recognized risk factor for cardiovascular disease. We suggest that disturbed water balance and hypernatremia increase vWF, resulting in increased risk of thrombosis. Supported by the Intramural Program of NHLBI