The early phase of the DCT manages the reabsorption of approximately 10-15% of filtered water, 5–10% of filtered sodium, and 5–10% of filtered chloride. This process is facilitated by Na⁺–Cl⁻ symporters in apical membranes and sodium-potassium pumps, as well as Cl⁻ leakage channels in basolateral membranes. The early DCT also stands out as a site where parathyroid hormone (PTH) stimulates calcium reabsorption, depending on the body's requirements.

The distal part of the DCT, along with the collecting duct, houses two types of cells - principal cells and intercalated cells. Principal cells are responsible for reabsorbing sodium and secreting potassium, while intercalated cells handle the reabsorption of bicarbonate and the secretion of hydrogen, thereby contributing to blood pH regulation.

In normal circumstances, the cells in the distal part of the DCT and the collecting ducts are practically impermeable to water. However, in response to elevated plasma osmolarity, such as during dehydration, or reduced blood volume, the hypothalamus triggers the release of antidiuretic hormone (ADH) from the posterior pituitary gland. ADH then binds to receptors on the principal cells in the distal DCT and collecting ducts, promoting the insertion of aquaporin-2 (AQP2) water channels into the apical membrane of these principal cells.

AQP2 channels exist as pre-formed channels inside cytoplasmic vesicles and mobilize to the cell membrane upon stimulation by ADH. With AQP2 now embedded in the membrane, water can pass from the tubular lumen into the cells. From there, water moves through basolateral aquaporins (AQP3 and AQP4) into the surrounding interstitial space and eventually into the bloodstream.

As a result, water reabsorption increases, concentrating the urine and helping to restore normal plasma osmolarity and blood volume.