Zusman R M, Keiser H R
Kidney Int. 1980 Mar;17(3):277-83. doi: 10.1038/ki.1980.33.
We investigated the regulation of cellular prostaglandin E2 (PGE2) biosynthesis in rabbit renomedullary interstitial cells in tissue culture. Arachidonic acid markedly stimulated PGE2 biosynthesis by these cells. Repeated exposure to arachidonic acid, resulted in progressively less stimulation of PGE2 biosynthesis. Potassium and dexamethasone diminished PGE2 biosynthesis by decreasing the rate of arachidonic acid release from the endogenous arachidonic acid storage pool. Hyperosmolality, like angiotensin II, bradykinin, and arginine vasopressin, stimulated PGE2 biosynthesis by increasing the rate of arachidonic acid release. Inhibitors of protein synthesis diminished angiotensin II-, bradykinin-, and arginine-vasopressin-stimulated PGE2 biosynthesis by decreasing hormone-stimulated arachidonic acid release. The effects of potassium, dexamethasone, arachidonic acid, and hyperosmolality on PGE2 biosynthesis were unaffected by protein synthesis inhibitors. Hormone-stimulated phospholipase activation is dependent on protein synthesis, whereas potassium, hyperosmolality, and dexamethasone alter the release of arachidonic acid from cellular lipids via a mechanism that is independent of protein synthesis.
我们在组织培养中研究了兔肾髓质间质细胞中细胞前列腺素E2（PGE2）生物合成的调节。花生四烯酸显著刺激这些细胞的PGE2生物合成。反复暴露于花生四烯酸会导致对PGE2生物合成的刺激逐渐减少。钾和地塞米松通过降低内源性花生四烯酸储存池中花生四烯酸的释放速率来减少PGE2生物合成。高渗状态与血管紧张素II、缓激肽和精氨酸加压素一样，通过提高花生四烯酸的释放速率来刺激PGE2生物合成。蛋白质合成抑制剂通过减少激素刺激的花生四烯酸释放来减少血管紧张素II、缓激肽和精氨酸加压素刺激的PGE2生物合成。钾、地塞米松、花生四烯酸和高渗状态对PGE2生物合成的影响不受蛋白质合成抑制剂的影响。激素刺激的磷脂酶激活依赖于蛋白质合成，而钾、高渗状态和地塞米松通过一种独立于蛋白质合成的机制改变细胞脂质中花生四烯酸的释放。
