Dahl salt-sensitive rats excrete 25-hydroxyvitamin D into urine.
The plasma 25-hydroxyvitamin D concentration of Dahl salt-sensitive rats (S) is markedly decreased in response to high sodium chloride (salt) intake. We tested the hypothesis that urinary excretion is a mechanism for the decrease. Female S rats excreted 0.26 +/- 0.04 nmol 25-hydroxyvitamin D/24 h at wk 2 of high salt (80 g/kg) intake, five times that of female salt-resistant (R) rats at wk 2 of high salt intake and nine times that of S rats at wk 2 of low salt (3 g/kg) intake. The 25-hydroxyvitamin D binding activity in 24-h urine of S rats was 79 +/- 11 pmol/h at wk 2 of high salt intake, two times that in urine of S rats at wk 2 of low salt intake and > 35 times that in urine of R rats at wk 2 of low or high salt intake. We conclude that markedly decreased plasma 25-hydroxyvitamin D concentrations of S rats during high salt intake result in part from excretion of protein-bound 25-hydroxyvitamin D. Low plasma 25-hydroxyvitamin D concentrations in humans may also result in part from salt sensitivity, which is prevalent in > 50% of the United States hypertensive population.
Thierry-Palmer
Myrtle
M
Department of Biochemistry, Morehouse School of Medicine, Atlanta, GA, USA. thierrm@msm.edu
Doherty
Akins
A
Bayorh
Mohamed A
MA
Griffin
Keri
K
D000818:Animals; D005260:Female; D051381:Rats; D020303:Rats, Inbred Dahl; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage*; D014807:Vitamin D / Q000031:analogs & derivatives* / Q000097:blood / Q000652:urine*
D017673:Sodium Chloride, Dietary; D014807:Vitamin D; C104450:25-hydroxyvitamin D