| タイトル | Renal Osteodystrophy in the Dahl Salt-Sensitive Rat |
| 著者（英） | Arnaud, S. B.; Savayongsa, P.; Zerath, E.; Thierry-Palmer, M.; DePaoli, A.; Cephas, S. |
| 著者所属（英） | NASA Ames Research Center |
| 発行日 | 2003-01-01 |
| 言語 | eng |
| 内容記述 | The Dahl salt-sensitive rat (SS) is a genetic model for human salt-sensitive hypertension in which we have found low circulating 25-hydroxyvitamin D (25-D) during high salt intake. We have reported deteriorating renal function with aging in one year-old S rats fed normal salt diets primarily (ASBMR, 2002). Kidneys were enlarged compared to salt-resistant (SR) controls and showed extensive nephrosclerosis and tubular atrophy, lesions not found in SR rats of the same age. The impairment in creatinine clearance was modest. Changes in the calcium endocrine system with aging in SS males were slight hypocalcemia, secondary hyperparathyroidism, low plasma 25-D and 24,25-D, and normal plasma 1,25-D. Significant 25-D, 25-D binding activity, and proteinuria three times that in the urine of SR rats, may have contributed to the low plasma 25-D and 24,25-D in SS rats. This study was undertaken to determine whether there was significant bone disease in this same group of rats. Ten SS and 13 SR rats were given calcein, 15 mg/kg, SQ, 7 and 3 days prior to necropsy for quantitative histomorphometry of the right tibia. The right femur was analyzed for mineral content. Ash weights were lower in SS than in SR femurs (470 plus or minus 22 vs. 497 plus or minus 25, p less than 0.01). Tibial bone volume was 12 plus or minus 3% of total volume in SS, but 17 plus or minus 2% in SR (p less than 0.001) and SS rats had fewer trabeculae. Osteoblasts covered three times the bone surface in SS as in SR tibiae and osteoclasts nearly twice the bone surface. Mineral apposition rates were delayed in SS compared to SR (1.6 plus or minus 0.3 vs. 1.3 plus or minus 0.1 um/d, p less than .003). There is clear evidence of bone disease in the male one-year old Dahl SS rats fed primarily normal salt diets. The main features of this bone disease incriminate the renal loss of 25-D, consequent low vitamin D status and secondary hyperparathyroidism in its pathogenesis. |
| NASA分類 | Inorganic, Organic and Physical Chemistry |
| 権利 | Copyright |
| URI | https://repository.exst.jaxa.jp/dspace/handle/a-is/333015 |
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