Parnova R G, Firsov D L
Biull Eksp Biol Med. 1991 Jan;111(1):5-7.
In experiments carried out on the frog urinary bladder, it was found that 20 sec after vasopressin was added, the content of 1,2-di-acylglycerol, labelled with [3H]-arachidonic acid, increased by 44% and the content of [3H]-phosphatidylinositol-4,5-diphosphate (PIP2) decreased by 22%. Five minutes after hormone addition the amount of prostaglandin E (PGE) released into the serosal solution was increased three-fold. Preincubation of bladders in 10(-4) M neomycin led to a 26% increase in vasopressin-stimulated water flow, a block of PIP2 breakdown, and a reduction in PGE synthesis of 62%. A significant decrease in content of lipids labelled with [3H]-arachidonic acid was found in 1,2-diacylglycerol and phosphatidylethanolamine (diacyl form). The data obtained suggest that the role of PIP2 breakdown products in negative feed-back regulation of the hydroosmotic action of vasopressin at least in part includes their connection with PGE biosynthesis activation.
在对青蛙膀胱进行的实验中发现,加入血管加压素20秒后,用[3H] - 花生四烯酸标记的1,2 - 二酰基甘油含量增加了44%,而[3H] - 磷脂酰肌醇 - 4,5 - 二磷酸(PIP2)含量下降了22%。加入激素五分钟后,释放到浆膜溶液中的前列腺素E(PGE)量增加了两倍。将膀胱在10(-4) M新霉素中预孵育导致血管加压素刺激的水流量增加26%,PIP2分解受阻,PGE合成减少62%。在1,2 - 二酰基甘油和磷脂酰乙醇胺(二酰基形式)中发现用[3H] - 花生四烯酸标记的脂质含量显著下降。所获得的数据表明,PIP2分解产物在血管加压素的水渗透作用的负反馈调节中的作用至少部分包括它们与PGE生物合成激活的联系。