A microperfusion study of phosphate reabsorption by the rat proximal renal tubule. Effect of parathyroid hormone

Abstract

To study the mechanism of phosphate reabsorption by the proximal tubule and the effect of parathyroid hormone (PTH), microperfusion experiments were carried out in rats. Segments of proximal tubule isolated by oil blocks were perfused in vivo with one of 3 solutions, each containing 152 meq/l Na+ and 2 mmol/l phosphate, but otherwise differing in composition. The pH of solution 1 was 6.05-6.63, indicating that 60-85% of the phosphate was in the form of H2PO4-. The pH of solution 2 was 7.56-7.85, and 85-92% of the phosphate was in the form of HPO42-. Solution 3 contained HCO3- and glucose and had a pH of 7.50-7.65. When the proximal tubules were perfused with solution 1, the 32P concentration in the collected perfusate was found to be consistently lower than in the initial perfusion solution. In sharp contrast, when the tubules were perfused with solutions 2 or 3, 32P concentration usually rose above that in the initial solution. Water (and presumably Na+) reabsorption, as measured with [3H]inulin, was the same with the acid and alkaline solutions. Administration of partially purified PTH clearly prevented the fall in phosphate concentration with the acid solution, but had a less discernible effect on phosphate reabsorption with the 2 alkaline solutions. Measurements of pH within the perfused segments with antimony microelectrodes demonstrated that PTH enhanced alkalinization of the acid perfusion solution. The findings are consistent with the view that H2PO4- is reabsorbed preferentially over HOP42-. This can be attributed to either an active transport mechanism for H2PO4- or selective membrane permeability to this anion. PTH appears to either inhibit an active transport process for H2PO4-, or to interfere with passive diffusion of phosphate by alkalinizing the tubular lumen.