Main points on physiological basis underlying AVP-D and AVP-R avoidance
| Mechanism | Description | Reference(s) |
|---|---|---|
| AVP release and function | AVP is produced by the hypothalamus and released by the posterior pituitary in response to increased plasma osmolality or dehydration. It promotes water reabsorption in the kidneys, concentrating urine. | [30, 31] |
| Countercurrent mechanism | The countercurrent multiplier in the loop of Henle and the exchanger in the vasa recta create a hyperosmotic gradient in the renal medulla, essential for water reabsorption in the presence of AVP. | [49, 51] |
| Regulation of urine concentration and dilution | In the presence of AVP, collecting ducts become permeable to water, allowing reabsorption and urine concentration. Without AVP, the ducts remain impermeable, leading to dilute urine. | [52] |
| AVP receptor activation | AVP binds to V2 receptors in the kidney’s collecting ducts, activating the cAMP-PKA pathway, which promotes water reabsorption. Proper receptor function prevents excessive water loss, as in AVP-D. | [34, 35] |
| AQP-2 channels | AVP triggers the movement of AQP-2 water channels to the collecting duct cells’ apical membrane, allowing water reabsorption. Proper AQP-2 function protects against AVP-R caused by channel disruption. | [56] |
| Maintenance of the medullary osmotic gradient | The countercurrent multiplier in the loop of Henle concentrates solutes, creating a gradient that facilitates water reabsorption under AVP influence. The exchanger helps preserve this gradient. | [57] |
| Solute transporters | Na+/K+/2Cl– co-transporters in the thick ascending limb of the loop of Henle establish the osmotic gradient, supporting urine concentration and preventing excessive water loss. | [58] |
AQP-2: aquaporin-2; AVP: arginine vasopressin; AVP-D: AVP deficiency; AVP-R: AVP resistance; cAMP-PKA: cyclic adenosine monophosphate-protein kinase A; V2: vasopressin 2