As the nephron dips into the medulla in the descending limb of the loop of Henle, water passively diffuses out of the filtrate. This concentrates the solutes in the filtrate. As the filtrate enters the ascending limb of the loop of Henle, the tube becomes impermeable to water and ions are pumped into the interstitium. This creates a gradient of higher ion concentration in the medulla and dilutes the filtrate.

The diluted filtrate enters the distal convoluted tubule, where water and ions are reabsorbed. This slightly increases the filtrate concentration before it enters the collecting duct. As the filtrate flows down the collecting duct into the renal medulla, the ions in the interstitium act to draw water out of the duct (dependent on the presence of antidiuretic hormone). The result is a highly concentrated urine product after the filtrate travels down the collecting duct, all due to the ion gradient established by the loop of Henle.

The loop of Henle is essential for creating an ion gradient in the renal medulla (the inner part of the kidney). In the descending limb of the loop of Henle, water is removed from the filtrate by aquaporin proteins (water channels). The result is a highly concentrated filtrate at the bottom of the loop.

The filtrate then enters the thick ascending limb, which is permeable to sodium ions. The sodium ions rush out of the filtrate into the interstitium, which now has lower concentration than the filtrate. When the collecting duct later travels through the high concentration of sodium ions that have accumulated in the renal medulla from the thick ascending limb, water is pulled out of the filtrate into the interstitium. This allows for the final step in concentrating the urine before it travels to the bladder.

Diuretic drugs promote the production of urine. One drug, known as furosemide, inhibits transport of both sodium and chloride in the ascending limb of the loop of Henle. This mechanism of action prevents the maintenance osmolarity gradients that promote the reabsorption of water, resulting in more dilute urine. If the gradient is lost, then water is not drawn out of the filtrate as it travels through the collecting duct and the result is a larger volume of dilute urine. Antidiuretic hormone, secreted from the posterior pituitary, works to promote the reabsorption of water in the collecting duct, which concentrates the urine and conserves water.

The loop of Henle serves the crucial function of creating an ion gradient in the renal medulla by fluctuating the reabsorption of water and ions. In the descending limb, water is removed from the filtrate and enters into the interstitium, resulting in a highly concentrated filtrate. This filtrate then enters the ascending limb. The ascending limb is not permeable to water, but is permeable to sodium ions. The result is a massive efflux of sodium ions, which exit the filtrate and enter the interstitium. Sodium pumps amplify this process by continuing to remove sodium from the filtrate. The filtrate becomes more dilute, but the interstitium in the renal medulla is highly concentrated. When the filtrate enters the collecting duct, this gradient helps pull water out of the filtrate, allowing it to reach a maximum concentration before being transported to the bladder.

If the ascending limb of the loop of Henle were permeable to water, this process would be impossible and the filtrate would not be concentrated in the collecting duct.          

Water is reabsorbed at various times during the excretion process as it passes through the nephron, in order to maintain proper ion levels. It is not, however, reabsorbed as urine ascends through the thin and thick ascending limbs in the loop of Henle. Rather, this region only involves ion reabsorption and urea secretion.

Sodium is reclaimed through passive transport in the thin ascending limb and is reclaimed by active transport in the thick ascending limb, distal tubule, and collecting duct. Each location of sodium resorption uses a different transport protein and mechanism.

The filtrate and surrounding interstitial fluid are at their highest osmolarities at the bottom of the loop of Henle. As the filtrate continues on, it enters the thin ascending limb of the loop of Henle, which is impermeable to water. As the thin ascending limb moves up through the nephron into areas with a lower osmolarity, sodium flows down its concentration gradient to exit the filtrate. At this point, the filtrate is at a lower osmolarity than the surrounding interstitial fluid due to sodium flowing out and water being barred from flowing in.

As filtrate travels down the descending limb of the loop of Henle, water passively leaves the filtrate as the descending limb passes through portions of the nephron that contain a more concentrated interstitial fluid. Water always travels from places of high water concentration (low osmolarity) to low water concentration (high osmolarity); thus, the water will passively flow out of the filtrate and into the interstitium.

As the loop of Henle turns, the filtrate passes through the thin ascending limb, which is impermeable to water, but permeable to ions. As the limb passes through less concentrated areas of the nephron, sodium passively flows down its concentration gradient from the filtrate to the interstitial fluid. At no point during this process is water actively transported.

In the presence of antidiuretic hormone (ADH), water is reabsorbed and the urine is concentrated. Antidiuretic hormone plays the biggest role on the collecting duct and distal tubule, allowing water to diffuse into the medulla by increasing the production of aquaporin proteins. These proteins become embedded in the membranes of the nephron epithelium and allow water to pass through the usually impermeable cells.

The other important regulator of water balance is aldosterone, which works by a different mechanism. Aldosterone increases production of sodium channels, allowing sodium to exit the filtrate in the distal tubule. Water diffuses to follow the reabsorbed sodium ions.

There are two main systems designed to regulate water reabsorption in the kidney: antidiuretic hormone (vasopressin) and the renin-angiotensin-aldosterone system (RAAS). The RAAS system includes a combination of substances that raise blood pressure through arteriole constriction and sodium reabsorption. It employs a specialized tissue that supplies blood to the glomerulus, called the juxtaglomerular apparatus (JGA), which produces the enzyme renin when stimulated by a drop in blood pressure.

Renin secretion is the first step in a series of reactions that serve to lower blood pressure. Renin enters the bloodstream, where it interacts with angiotensinogen and produces angiotensin I. Angiotensin-converting enzyme in the lungs further converts angiotensin I into angiotensin II. Angiotensin II has two primary functions: it acts as vasoconstrictor and stimulates release of aldosterone from the adrenal cortex. Vasoconstriction helps to immediately increase local blood pressure. Aldosterone interacts with the distal tubule of the nephron to increase sodium reabsorption. The increase in interstitial osmolarity helps pull water out of the filtrate, concentrating the urine and enhancing water conservation, which can increase blood volume and pressure.

Atrial natriuretic hormone serves to inhibit the RAAS system when blood pressure is low.

Vasopressin, also called antidiuretic hormone (ADH), is part of the hormonal control of urine excretion and functions to enhance water reabsorption and limit the excretion of water in urine. Vasopressin is released when osmoreceptor cells in the hypothalamus detect a rise in the osmolarity or solute concentration of the blood above a threshold level.

Conversely, intake of a large quantity of water will lower blood osmolarity and signal that water conservation is not needed. When blood volume or pressure increases and blood osmolarity decreases, production of vasopressin is inhibited in order to promote water excretion.