The cortical collecting duct is where all of the distal tubules of the nephrons in the kidneys feed. It is fed by many nephrons, and is the last chance for the kidney to reabsorb or excrete any of the filtrate before it enters the renal pelvis and is later excreted via micturation.

Angiotensin II causes sodium and chloride reabsorption in the collecting duct, as well as in the distal tubule. Its permeability to water is controlled by antidiuretic hormone (or vasopressin, as it is also known). Water reabsorption is aided by the duct's positioning within the renal medulla, where the interstitial side of the membrane has a very high osmolality (hyperosmolality). This draws water back in when the membrane is permeable to it, via osmotic pressure. This increased permeability is due to the insertion of more aquaporin proteins in the membrane upon binding of vasopressin.

The collecting duct also reabsorbs urea, and excretes around 30 percent of the absorbed potassium. The potassium absorption in the collecting duct is due to potassium-specific ion channels, and is passive. Regulation in the duct is active, and is done via sodium-potassium ATPase.

These are my interpretation of my lecture notes, but I may have used some references from Hole's Anatomy and Physiology (Shier, Butler, Lewis) and Human Physiology (Vander, Sherman, Luciano)

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