Master Collecting Duct with Picmonic for Medicine

Aldosterone, a mineralocorticoid secreted by the adrenal cortex (zona glomerulosa), acts on principal cells in the collecting duct. It increases the expression of:
Na⁺/K⁺ ATPase pumps on the basolateral membrane (pumping Na⁺ into the blood and K⁺ into the cell)
Epithelial sodium channels (ENaC) on the luminal membrane allow Na⁺ reabsorption from the tubular lumen.
This active sodium reabsorption is coupled with potassium secretion into the lumen.
Aldosterone release is stimulated by angiotensin II, hyperkalemia, and ACTH (to a minor degree).

Vasopressin (antidiuretic hormone, ADH), released from the posterior pituitary, acts on V₂ receptors in the collecting duct. Activation of these receptors increases aquaporin-2 (AQP2) channel insertion on the apical membrane of principal cells.
This allows water reabsorption from the tubular lumen into the hyperosmolar medullary interstitium, concentrating the urine.
The osmotic gradient that drives this process is generated by the loop of Henle and maintained by urea recycling in the inner medullary collecting duct.

The collecting duct is responsible for the final concentration of urine. As the tubular fluid descends through the medulla, the high osmotic gradient created by NaCl and urea allows water reabsorption (under ADH influence), reducing urine volume and increasing solute concentration.