AVP, also known as vasopressin, plays a crucial role in increasing the permeability of the inner medullary collecting duct to urea. This leads to enhanced urea reabsorption and an increase in the osmolality of the medullary interstitial fluid, which is essential for optimal urine concentration. The cells of the collecting duct express two types of urea transporters: UT-A1 and UT-A3. UT-A1 is found on the apical membrane, while UT-A3 is primarily located on the basolateral membrane. AVP, through the cAMP/PKA cascade, promotes the expression of both UT-A1 and UT-A3. Additionally, increasing the osmolality of the medullary interstitial fluid also boosts the permeability of the inner medullary collecting duct to urea. This effect is mediated by the phospholipase C/protein kinase C (PKC) pathway, which increases the expression of UT-A1 and UT-A3.

AVP also stimulates the reabsorption of NaCl by the thick ascending limb of Henle's loop, as well as the distal tubule and cortical segment of the collecting duct. This increase in Na+ reabsorption is associated with an increased abundance of three Na+ transporters: the 1Na+/1K+/2Cl− symporter in the thick ascending limb of Henle's loop, the Na+/Cl− symporter in the distal tubule, and the Na+ channel (ENaC) in the latter portion of the distal tubule and collecting duct. Stimulation of NaCl transport in the thick ascending limb helps maintain the hyperosmotic medullary interstitium necessary for water absorption from the medullary portion of the collecting duct.

Changes in plasma osmolality, blood volume, or pressure not only affect AVP secretion but also impact the perception of thirst. An increase in body fluid osmolality or a decrease in blood volume or pressure triggers the sensation of thirst. Among these stimuli, hypertonicity is more potent. Even a small increase in plasma osmolality of 2% to 3% strongly stimulates the desire to drink, whereas a decrease in blood volume or pressure of approximately 10% to 15% is required to produce the same response.

As mentioned earlier, there is a genetically determined threshold for AVP secretion and a separate threshold for triggering thirst. However, the thirst threshold is higher than the threshold for AVP secretion. On average, the threshold for AVP secretion is around 285 mOsm/kg H2O, while the thirst threshold is approximately 295 mOsm/kg H2O. This means that thirst is stimulated at a body fluid osmolality where AVP secretion is already at its maximum.

The neural centers responsible for regulating water intake (the thirst center) are located in the same region of the hypothalamus involved in regulating AVP secretion. However, it remains uncertain whether the same cells serve both functions. Nonetheless, the thirst response, like the regulation of AVP secretion, is a complex process that plays a vital role in maintaining fluid balance.
AVP also increases the permeability of the terminal portion of the inner medullary collecting duct to urea. This results in an increase in urea reabsorption and an increase in the osmolality of the medullary interstitial fluid, which as described below is needed for maximal urine concentration. The cells of the collecting duct express two types of urea transporters, UT-A1 and UT-A3. UT-A1 is localized to the apical membrane, and UT-A3 is localized primarily to the basolateral membrane. AVP, acting through the cAMP/PKA cascade, increases expression of both UT-A1 and UT-A3. Increasing the osmolality of the interstitial fluid of the renal medulla also increases the permeability of the inner medullary collecting duct to urea. This effect is mediated by the phospholipase C/protein kinase C (PKC) pathway, which increases UT-A1 and UT-A3 expression.
AVP also stimulates reabsorption of NaCl by the thick ascending limb of Henle’s loop and by the distal tubule and cortical segment of the collecting duct. This increase in Na+ reabsorption is associated with increased abundance of three Na+ transporters: the 1Na+/1K+/2Cl− symporter (thick ascending limb of Henle’s loop), the Na+/Cl− symporter (distal tubule), and the Na+ channel (ENaC, in the latter portion of the distal tubule and collecting duct). Stimulation of thick ascending limb NaCl transport may help maintain the hyperosmotic medullary interstitium that is necessary for absorption of water from the medullary portion of the collecting duct (see below).
In addition to affecting the secretion of AVP, changes in plasma osmolality and blood volume or pressure lead to alterations in the perception of thirst. When body fluid osmolality is increased or the blood volume or pressure is reduced, the individual perceives thirst. Of these stimuli, hypertonicity is the more potent. An increase in plasma osmolality of only 2% to 3% produces a strong desire to drink, whereas decreases in blood volume and pressure in the range of 10% to 15% are required to produce the same response.
As already discussed, there is a genetically determined threshold for AVP secretion (i.e., a body fluid osmolality above which AVP secretion increases). Similarly there is a genetically determined threshold for triggering the sensation of thirst. However, the thirst threshold is higher than the threshold for AVP secretion. On average the threshold for AVP secretion is approximately 285 mOsm/kg H2O, whereas the thirst threshold is approximately 295 mOsm/ kg H2O. Because of this difference, thirst is stimulated at a body fluid osmolality where AVP secretion is already maximal.
The neural centers involved in regulating water intake (the thirst center) are located in the same region of the hypothalamus involved with regulating AVP secretion. However, it is not certain whether the same cells serve both functions. Indeed the thirst response, like the regulation of