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Nutrient Interactions and Toxicity
Research Communication

Dahl Salt-Sensitive Rats Excrete 25-Hydroxyvitamin D into Urine^1,2

Departments of Biochemistry and ^* Pharmacology/Toxicology, Morehouse School of Medicine, Atlanta, GA

³To whom correspondence should be addressed. E-mail: thierrm{at}msm.edu.

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.

KEY WORDS: • salt sensitivity • vitamin D • Dahl rats • sodium chloride