Popovtzer M M, Robinette J B
Am J Physiol. 1975 Oct;229(4):907-10. doi: 10.1152/ajplegacy.1975.229.4.907.
To further evaluate the effect of 25(OH)vitamin D3 (25(OH)vit D3) on renal handling of phosphorus, fractional excretion of phosphorus (CP/CIn) and urinary excretion of cyclic AMP (UcAMP) were measured in the following groups of animals: 1) intact rats receiving intravenously 25(OH)vit D3. 2a) Parathyroidectomized (PTX) rats receiving a continuous infusion of parathyroid hormone (PTH). 2b) PTX rats undergoing continuous infusion of PTH and receiving intravenously 25(OH)vit D3. In group 1 a decrease in CP/CIn from a control value of 0.210 +/- 0.064 (kappa +/- SE) to 0.052 +/- 0.017 (P less than 0.001) during 25(OH)vit D3 infusion was associated with a corresponding decrease in UcAMP from 182 +/- 18 to 87 +/- 8 pmol/min (P less than 0.001). In group 2a an increase in CP/CIn from a control value of 0.031 +/- 0.014 to 0.365 +/- 0.017 during PTH infusion was associated with a corresponding increase in UcAMP from 76 +/- 17 to 330 +/- 51 pmol/min (P less than 0.001). In group 2b a decrease in CP/CIn from 0.365 +/- 0.017 to 0.256 +/- 0.011 (P less than 0.01) during 25(OH)vit D3 infusion was associated with a decrease in UcAMP from 356 +/- 63 to 191 +/- 33 pmol/min (P less than 0.01). These results indicate that the blunting of the phosphaturic response to PTH by 25(OH)vit D3 is associated with a decrease in UcAMP. This observation suggests that the mechanism underlying the enhanced tubular reabsorption of phosphorus is inhibition of the PTH-induced activation of adenylate cyclase in the kidney.