论文部分内容阅读
垂体加压素(vasopressin)及其九肽结构类似物催产素(oxytocin)经肝细胞V_1受体和跨膜信号传递系统,通过增加肝细胞内钙离子浓度而诱导肝磷酸化酶α活性,催化肝糖原的分解代谢.在正常生理条件下,细胞膜表面特异性受体数目受机体内环境的影响,通过上行或下行调节偶联受体-效应反应. 实验采用大鼠脱水模型,比较上述激素在不同脱水时期的糖原分解作用,结果证明在生理条件下加压素对肝细胞特异性受体有下行调节作用. 大鼠脱水96h后,血浆渗透压由正常时285±1mOsm/kg增至316±3mOsm/kg(P<0.001),血浆血
Pituitary vasopressin and its nonapeptide structural oxytocin induce hepatic phosphorylase α activity by increasing hepatic intracellular calcium concentration via V 1 receptor and transmembrane signal transduction system. Hepatic glycogen catabolism Under normal physiological conditions, the number of cell-surface-specific receptors is influenced by the environment in the body and the up-regulation or down-regulation of the coupled receptor-response is used.The rat dehydration model was used to compare the above hormones The results showed that vasopressin had a downward regulatory effect on hepatocyte-specific receptors under physiological conditions.Plasma osmolality was increased from normal to 285 ± 1 mOsm / kg after 96 h of dehydration 316 ± 3 mOsm / kg (P <0.001), plasma blood