Unidirectional duodenal and jejunal calcium and phosphorus transport in the rat: Effects of dietary phosphorus depletion, ethane-1-hydroxy-1,1-diphosphonate and 1,25 dihydroxycholecalciferol

Summary

Unidirectional calcium (Ca) and phosphorus (Pi) transport was studied in vitro by means of a modified Ussing technique in the absence of electrochemical gradients between the mucosal and serosal buffer medium. Duodenum and jejunum of male albino Sprague-Dawley rats were investigated after Pi depletion alone (0.03% diet-Pi), Pi depletion and EHDP treatment (40 mg/kg per day s.c. × 4), and Pi depletion, EHDP and 1,25(OH)₂D₃ (500 pmol i.v. × 2) treatment. Mucosal-to-serosal Ca and Pi fluxes (Jms) changed in parallel, depending on the 1,25(OH)₂D₃-status of the animals. Regarding serosal-to-mucosal fluxes (Jsm), Pi depletion resulted in an increase in Jsm for Ca and Pi, associated with a rise in Gt and Isc in the duodenum but not in the jejunum. EHDP administered to block synthesis of 1,25(OH)₂D₃ caused further augmentation in duodenal Jsm for calcium but not phosphorus, which was paralleled by an increase in Gt and Isc. After repletion with 1,25(OH)₂D₃, an increase in Jsm for Ca and Pi and a rise in Gt and Isc were observed in the duodenum and in the jejunum. Serosal-to-mucosal fluxes for Ca and Pi were related to tissue conductance (Gt) in the duodenum (r = 0.89,P < 0.001 andr = 0.84;P < 0.001, respectively), as well as in the jejunum (r = 0.55;P < 0.01 andr = 0.66;P < 0.001, respectively). Changes in Jsm also paralleled changes in transmural shortcircuit current (Isc). The data are compatible with the assumption of an increase in Jsm for Ca and Pi and a rise in Gt, both reflecting an increase in water recycling across the tight junctions caused by a rise in sodium absorption. They provide further evidence that the overall effect of 1,25(OH)₂D₃ on intestinal Ca and Pi transport is to increase both cell-mediated active mucosal-to-serosal transport and paracellular diffusional serosal-to-mucosal ion movement.