Potentiation by calcium of the proximal tubular transport effects of parathyroid hormone.

Previous studies from this laboratory have demonstrated that a low ('physiological') dose of parathyroid hormone (PTH) effects a phosphaturia in chronically thyroparathyroidectomized (TPTX), hypocalcemic dogs, similar in magnitude to that seen in normal intact animals, without altering proximal tubular reabsorption. In addition, cyclic AMP did not increase following this amount of PTH, despite the phosphaturia. Since calcium is an important modulator of transport events, we studied the effects of restoring serum calcium (Ca) to normal before administering a physiological dose of PTH (0.3-0.5 U/kg). In hypocalcemic dogs given only physiological amounts of PTH, percentage phosphate excretion (%EPO4) rose from 3.81 +/- 1.48 to 18.29 +/- 5.69% (p less than 0.025) without any alteration in proximal tubular function. Ca infusion alone likewise did not change %EPO4 or proximal tubular transport. However, calcium-infused dogs given a physiological dose of PTH showed a reduction in proximal tubular fractional phosphate reabsorption from 0.73 +/- 0.04 to 0.63 +/- 0.04 (p less than 0.005), as well as an increase in %EPO4 (from 5.64 +/- 1.69 to 15.86 +/- 2.82%, p less than 0.001), without any increase in urinary or tissue cyclic AMP. We conclude that the elevation of the serum Ca to normal restores the ability of PTH in physiological amounts to alter proximal tubular PO4 transport. The data also suggest that this action of PTH is mediated by Ca, rather than by the adenylate cyclase system.