Plasma 24,25-dihydroxyvitamin D concentration of Dahl salt-sensitive rats decreases during high salt intake

• Published in: The Journal of steroid biochemistry and molecular biology 2002-03, Vol.80 (3), p.315-321
• Main Authors: Thierry-Palmer, Myrtle, Tewolde, Teclemicael K., Forté, Camille, Wang, Min, Bayorh, Mohamed A., Emmett, Nerimiah L., White, Jolanda, Griffin, Keri
• Format: Article
• Language: English
• Subjects: 24,25-Dihydroxyvitamin D 3 - blood; Animals; Biological and medical sciences; Blood Pressure; Dahl rats; Fundamental and applied biological sciences. Psychology; Hypertension; Life Sciences (General); Rats; Salt-sensitivity; Sodium Chloride - pharmacology; Space life sciences; Steroid hormones. Cholecalciferol derivatives; Vertebrates: endocrinology; Vitamin D
• ISSN: 0960-0760; 1879-1220
• DOI: 10.1016/S0960-0760(02)00029-8

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) 2D) 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) 2D 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) 2D 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) 2D 3), administered at a level that increased plasma 24,25-(OH) 2D concentration to five times normal, did not attenuate the salt-induced hypertension of salt-sensitive rats. Plasma 24,25-(OH) 2D 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) 2D 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.