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

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Abstract
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.