Sato M, Dunn M J, Abe K, Yoshinaga K
Jpn Circ J. 1985 Sep;49(9):1012-8. doi: 10.1253/jcj.49.1012.
To investigate the relationship of renal prostaglandin E2 (PGE2) synthesis to medullary interstitial osmolality, rat renal papillary collecting tubule (RPCT) cells in culture were exposed to media with different osmolaties. PGE2 released into the media was measured by radioimmunoassay. Increasing osmolality with equiosmolar sodium chloride and urea from 300 to 900 mOsm slightly increased PGE2 synthesis, whereas further increase above 1200 mOsm markedly inhibited PGE2 synthesis in RPCT cells. Hyperosmolar media also inhibited calcium ionophore-stimulated PGE2 synthesis, but did not inhibit arachidonate-stimulated PGE2 synthesis. In contrast, decreasing osmolality from 1800 to 300 mOsm induced a prominent but transient increase in PGE2 synthesis. This increase was abolished by TMB-8, an intracellular calcium antagonist, and trifluoperazine, a calmodulin antagonist. Osmolar increments with sodium chloride or urea alone resulted in the similar inhibition of PGE2 synthesis by sodium chloride but not by urea. These results indicate that extracellular sodium chloride inhibits PGE2 synthesis in RPCT cells at the step of arachidonic acid release, possibly at phospholipases, in a calcium-dependent manner.
为研究肾前列腺素E2（PGE2）合成与髓质间质渗透压的关系，将培养的大鼠肾乳头集合管（RPCT）细胞置于不同渗透压的培养基中。采用放射免疫分析法测定培养基中释放的PGE2。用等渗的氯化钠和尿素将渗透压从300 mOsm提高到900 mOsm时，PGE2合成略有增加，而渗透压进一步升高至1200 mOsm以上时，明显抑制RPCT细胞中的PGE2合成。高渗培养基也抑制钙离子载体刺激的PGE2合成，但不抑制花生四烯酸刺激的PGE2合成。相反，将渗透压从1800 mOsm降至300 mOsm会导致PGE2合成显著但短暂增加。这种增加可被细胞内钙拮抗剂TMB - 8和钙调蛋白拮抗剂三氟拉嗪消除。单独用氯化钠或尿素增加渗透压时，氯化钠会对PGE2合成产生类似的抑制作用，而尿素则不会。这些结果表明，细胞外氯化钠在花生四烯酸释放步骤（可能在磷脂酶处）以钙依赖方式抑制RPCT细胞中的PGE2合成。
