The effects of acute phosphate depletion on isolated chick kidney tubule cells

Abstract

Isolated tubule cells from chick kidney respond to a short period of phosphate deprivation with increased phosphate uptake and a resistance to parathyroid hormone. During phosphate depletion a considerable amount of phosphate may be released from the cells, but intracellular inorganic phosphate levels are maintained by the hydrolysis of organic phosphate esters. It is suggested that the concomitant changes in metabolism might act as the signal causing the onset of the changes in phosphate handling associated with phosphate deprivation.

Study of the mechanism by which the Na+-Pi co-transporter of mouse kidney proximal-tubule cells adjusts to phosphate depletion

“…Diffusional uptake, measured in the absence of Na+, occurs at an identical rate in normal and depleted cells, however, suggesting that the cells differ little with respect to cytosolic Pi concentration. Indeed, when measurements have been made of cytosolic P1 in a number of cell types, it has been found that the anion concentration is not greatly influenced by the concentration of Pi in the surrounding medium (Bevington et al, 1986;Grahn & Butterworth, 1986). It seems that cytosolic Pi is buffered at the expense of organic phosphate and/or mitochondrial Pi, perhaps.…”

“…Isolated chick proximal-tubule cells (Grahn & Butterworth, 1986) and the kidney epithelial-cell line LLC-PK1 (Caverzasio et al, 1985) respond to a direct stimulus of low ambient Pi with an increase in Na+-dependent Pi uptake. These preparations are believed to provide a model for the transporter of the brushborder membrane of the proximal tubule of the intact kidney, and their stimulation by low Pi therefore suggests that other humoral factors are not involved directly in the process whereby kidney re-absorption of Pi is adjusted to meet the physiological demand for the anion.…”