In the intestine, both absorption and secretion of phosphate occur. Most of the dietary phosphate is absorbed in the duodenum and jejunum. Approximately 200 mg of phosphate is secreted into the gastrointestinal tract, mainly into saliva and bile. The net result is that about 65 % of phosphate is absorbed in the gastrointestinal tract. Two important mechanisms seem to participate in this process. One, localized in the duodenum, is a Na⁺-dependent secondary active transport system. The transporter involved in phosphate transport is called Na/Pi-type II_b cotransporter. It is influenced by a number of factors. Arsenate, mercury, and calcitonin inhibit, whereas 1,25(OH)₂D₃ and low phosphate diet stimulate this cotransporter. The second mechanism is phosphate-dependent, and is located in the jejunum and ileum. Phosphate absorption in these segments of the intestine depends on the luminal phosphate concentration. Absorption seems to be predominantly passive under normal circumstances and occurs through the paracellular pathway. As stated above, active transport becomes prominent when dietary phosphate is extremely low. Ca²⁺, Mg²⁺, and aluminum are important elements that complex with phosphate and decrease its intestinal absorption. These compounds are thus used to treat increased plasma [Pi] in clinical practice.

Under normal conditions, the exchange of phosphate between the bone and the extracellular pool is rather small (see Fig. 20.1), and the release of phosphate is always accompanied by the release of Ca²⁺. Thus, the release of phosphate is stimulated by the same hormones that stimulate the release of Ca²⁺.

The kidneys play a significant role in the maintenance of phosphate homeostasis. Since the dietary intake of phosphate varies daily, the total body phosphate concentration would also vary were it not for the kidneys. The kidneys vary their excretion of phosphate to the varying amounts of phosphate absorption by the intestine to maintain normal serum [Pi] .