抗利尿激素调节的水重吸收
中文名称
通路描述
在肾脏中，抗利尿激素（AVP）是调节水稳态的关键调节剂，通过控制从管腔到间质的水分移动来实现水重吸收，并调节尿水的排泄。在正常生理状态下，AVP 由后叶垂体分泌入血液循环，以血清渗透压增加或有效循环血量减少为响应。当到达肾脏时，AVP 结合到集合管上皮细胞基底侧的 V2 受体上，触发 G 蛋白偶联信号级联反应，导致水通道蛋白 2（AQP2）囊泡插入到顶部的细胞膜。这导致集合管的水通透性增加，在渗透梯度驱动下，原尿通过 AQP2 穿过膜，并通过 AQP3 和 AQP4 水通道离开细胞，这些水通道在细胞基底侧是常表达。当渗透压恢复时，降低的血浆 AVP 水平导致 AQP2 内化，使顶膜再次致密。
英文描述
In the kidney, the antidiuretic hormone vasopressin (AVP) is a critical regulator of water homeostasis by controlling the water movement from lumen to the interstitium for water reabsorption and adjusting the urinary water excretion. In normal physiology, AVP is secreted into the circulation by the posterior pituitary gland, in response to an increase in serum osmolality or a decrease in effective circulating volume. When reaching the kidney, AVP binds to V2 receptors on the basolateral surface of the collecting duct epithelium, triggering a G-protein-linked signaling cascade, which leads to water channel aquaporin-2 (AQP2) vesicle insertion into the apical plasma membrane. This results in higher water permeability in the collecting duct and, driven by an osmotic gradient, pro-urinary water then passes the membrane through AQP2 and leaves the cell on the basolateral side via AQP3 and AQP4 water channels, which are constitutively expressed on the basolateral side of these cells. When isotonicity is restored, reduced blood AVP levels results in AQP2 internalization, leaving the apical membrane watertight again.
所含基因
44 个基因