Corticopapillary Osmotic Gradient

The corticopapillary osmotic gradient is the osmotic gradient of the renal interstitium. It allows the nephrons to adjust the osmolarity of the tubular fluid, and ranges from 300 milliosmoles/liter in the cortex to up to 1200 milliosmoles in the inner medulla The physiological processes that create the gradient are: Medullary countercurrent multiplication & Urea recycling. Maintenance of the corticopapillary osmotic gradient relies on the vasa recta and countercurrent exchange. Parts of the nephron:

• Renal corpuscle
• Proximal tubule
• Nephron loop, specify its descending and ascending limbs; recall that the ascending limb is impermeable to water.
• Distal tubule
• Collecting duct

The nephron is surrounded by the renal interstitium, which comprises tissues and fluids.

• The corticomedullary junction marks where the cortex becomes the medulla.
• The proximal and distal tubules lie within the cortex, and the nephron loop lies within the medulla.
• The corticopapillary osmotic gradient (the osmolarity of the interstitium) increases from the cortex to the medulla.

The thick ascending limb actively pumps sodium chloride into the medullary interstitium to create the osmotic gradient: Isosmotic tubular fluid enters the descending limb of the nephron loop; its osmolarity is similar to that of blood plasma, 300 milliosmoles/liter. Water is passively reabsorbed in the descending limb; consequently, by the time it reaches the bend of the nephron loop, the tubular fluid is hyperosmotic, with osmolarity as high as 1200 milliosmoles/liter; this is because water has left the tubular fluid; solutes have not been added to the tubular fluid. The hyperosmotic tubular fluid is "pushed" into the ascending limb by the arrival of new tubular fluid; recall that tubular fluid is constantly flowing through the nephrons. Then, as it passes through the ascending limb, sodium chloride is actively reabsorbed from the tubular fluid, which lowers its osmolarity. Thus, as it exits the nephron loop, the tubular fluid is hypo-osmotic, at approximately 100 milliosmoles/liter. In other words, the nephron loop has created relatively dilute urine. Interstitial fluid of the cortex is isosmotic with blood plasma, at 300 milliosmoles/liter. Osmolarity increases incrementally as we move towards the inner medulla, where, like the tubular fluid, its osmolarity can be as high as 1200 milliosmoles/liter. This gradient is created by the continuous reabsorption of water and sodium chloride in the nephron loop: Recall that, because water was reabsorbed in the descending limb, the tubular fluid that enters the ascending limb has a very high solute concentration; Higher tubular fluid solute concentration leads to increased solute reabsorption, which raises the osmolarity of the medullary interstitium. However, as the tubular fluid ascends through the outer medulla and cortex, continuous solute reabsorption reduces its osmolarity. Thus, less solutes are available for transport to the interstitium, so its osmolarity decreases as we move superficially. Urea is reabsorbed from the medullary collecting ducts and contributes to the corticopapillary osmotic gradient. Urea reabsorption relies on the presence of anti-diuretic hormone (ADH, aka, arginine, vasopressin), thus it is most prominent in water depletion states: when circulating ADH levels are high. ADH increases water permeability, but has no effect on urea transport. As a result of water reabsorption, urea concentration in the tubular fluid increases. Then, in the inner medullary collecting duct, indicate that ADH increases both water permeability and urea transport; The diffusion of urea into the interstitial fluid increases the osmolarity of the inner medulla, which adds to the corticopapillary osmotic gradient. Urea can be secreted into the nephron loop, or, taken up by the vasa recta.