Increased urinary calcium excretion potentiates bone turnover in oophorectomized rats.

The differential effects of sodium-induced renal hypercalciuria on the biochemical markers of bone metabolism and calcium homeostasis were studied in oophorectomized (Oophx) and sham-operated rats. The rats consuming a normal (0.4%) calcium semisynthetic diet were randomly allocated to either 0, 0.4, 0.6, 0.9, or 1.25% NaCl in their drinking water for 7 days. At that time fasting blood and urine specimens were collected and analyzed for bone-related biochemical variables. The urinary calcium/creatinine ratio was increased with increasing urinary sodium (p < 0.01) in both sham and Oophx animals. The hydroxyproline/creatinine ratio was elevated as a result of Oophx (p < 0.001) and was raised with increasing urinary sodium in both sham (p = 0.012) and Oophx animals (p = 0.007). Serum osteocalcin and alkaline phosphatase were elevated in Oophx rats (p < 0.02). While serum osteocalcin was raised with increasing urinary sodium in Oophx rats (p = 0.035), there was no effect on osteocalcin levels in sham-operated rats. This study demonstrates that sodium-induced renal hypercalciuria potentiates bone turnover in Oophx rats as compared with ovary-intact rats and indicates important implications for the effect of dietary salt on bone turnover with ovarian hormone deficiency.