2/16/2023 0 Comments Graphpad prism 6 free download![]() ![]() In about 55% of the patients treated with lithium, the AQP2 redistribution is inhibited. ![]() DI can also be acquired, for example, as a consequence of lithium therapy of bipolar disorder. When the collecting duct principal cells cannot respond to the hormone due to mutations in the genes encoding the V2R or AQP2, the result is nephrogenic DI. 15– 18 If the hormone is absent as a consequence of mutations in the encoding gene, the disease is classified as central DI. Patients with DI produce large amounts of hypotonic urine and polydipsia. Vice versa, defects of the system cause diabetes insipidus (DI). When AVP levels are increased, such as in the syndrome of inappropriate antidiuretic hormone secretion, late-stage heart failure, or hepatic cirrhosis, AQP2 is predominantly located in the plasma membrane and causes excessive water retention, leading to hyponatremia. 11– 14ĭysregulation of AVP-mediated water reabsorption is associated with or causes disease. The inhibition causes depolymerization of F-actin and the removal of the barrier, facilitating the redistribution of AQP2 to the plasma membrane. AVP induces the protein kinase A (PKA)–mediated phosphorylation of RhoA at S188 and provides for its inhibition. RhoA maintains F-actin as a physical barrier, preventing AQP2-bearing vesicles from reaching the plasma membrane and thus, avoiding inappropriate water reabsorption under resting conditions. The AVP-induced redistribution of AQP2 is also associated with the inhibition of the small GTPase, RhoA. 4 This shift is associated with changes in the phosphorylation of serine 256 (S256), S264, and S269 of AQP2 as well as a decrease in the phosphorylation of S261 and a reduction in ubiquitination. V2R stimulation shifts this equilibrium toward plasma membrane localization. 1– 3 AQP2 constitutively recycles between its intracellular and plasma membrane localization. The plasma membrane insertion increases the osmotic water permeability of the collecting duct and facilitates water reabsorption from primary urine. ![]() The binding of antidiuretic hormone (arginine-vasopressin ) to its cognate V2 receptors (V2Rs) on the surface of renal collecting duct principal cells leads to the redistribution of the water channel aquaporin-2 (AQP2) from intracellular vesicles into the plasma membrane.
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