RESUMEN
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.
Asunto(s)
Cloruro de Sodio Dietético/administración & dosificación , Vitamina D/análogos & derivados , Vitamina D/orina , Animales , Femenino , Ratas , Ratas Endogámicas Dahl , Vitamina D/sangreRESUMEN
Dahl salt-sensitive rats, but not salt-resistant rats, develop hypertension in response to high salt intake. We have previously shown an inverse relationship between plasma 25-hydroxyvitamin D (25-OHD) concentration and blood pressure of Dahl salt-sensitive rats during high salt intake. In this study, we report on the relationship between high salt intake and plasma 24,25-dihydroxyvitamin D (24,25-(OH)(2)D) concentration of Dahl salt-sensitive and salt-resistant rats. Rats were fed a high salt diet (8%) and sacrificed at day 2, 7, 14, 21, and 28. Plasma 24,25-(OH)(2)D concentrations of salt-sensitive rats were reduced to 50% of that at baseline at day 2-when blood pressure and plasma 25-OHD concentration were unchanged, but 25-OHD content in the kidney was 81% of that at baseline. Plasma 24,25-(OH)(2)D concentration was reduced further to 10% of that at baseline from day 7 to 14 of high salt intake, a reduction that was prevented in rats switched to a low salt (0.3%) diet at day 7. Exogenous 24,25-dihydroxycholecalciferol (24,25-(OH)(2)D(3)), administered at a level that increased plasma 24,25-(OH)(2)D concentration to five times normal, did not attenuate the salt-induced hypertension of salt-sensitive rats. Plasma 24,25-(OH)(2)D concentration of salt-resistant rats was gradually reduced to 50% of that at baseline at day 14 and returned to baseline value at day 28 of high salt intake. We conclude that the decrease in plasma 24,25-(OH)(2)D concentration in salt-sensitive rats during high salt intake is caused by decreased 25-OHD content in the kidney and also by another unidentified mechanism.