Merenich J A, Sjoberg R J, O'Barr T P, Kidd G S
Department of Medicine and Biochemistry, Fitzsimons Army Medical Center, Aurora, CO 80045.
Prostaglandins. 1992 Aug;44(2):111-7. doi: 10.1016/0090-6980(92)90072-2.
Glucocorticoids are known inhibitors of prostaglandin production. Prostaglandin E2 (PGE2) and prostacyclin (PGI2) are promoters of natriuresis and renin release. Excessive prostaglandin production, therefore, might contribute to the altered sodium balance and renin release observed in primary adrenal insufficiency. To test this hypothesis, sodium balance and prostaglandin production were measured in adrenalectomized rats and in animals receiving prostaglandin inhibitors or replacement dexamethasone. Compared to sham-operated controls, adrenalectomized rats had decreased two-day sodium balance and elevated plasma renin concentration (PRC), renal PGE2 production, and renal 6-ketoprostaglandin F1 alpha (6kPGF1 alpha, the nonenzymatic metabolite of PGI2); however, no appreciable change in aortic 6kPGF1 alpha production was observed. Dexamethasone given to adrenalectomized rats normalized PRC but had no effect on sodium balance or prostaglandin production. Likewise, prostaglandin inhibitors did not alter the sodium balance or decrease the PRC post adrenalectomy. These data confirm renal prostaglandin production is increased in adrenalectomized rats, but suggest that the elevation is not due directly to glucocorticoid deficiency. Further, PRC levels in adrenal insufficiency do not appear to be prostaglandin mediated. In conclusion, excessive renal prostaglandin production does not contribute to altered sodium balance or increased PRC in adrenalectomized rats.
糖皮质激素是已知的前列腺素生成抑制剂。前列腺素E2（PGE2）和前列环素（PGI2）是利钠和肾素释放的促进剂。因此，前列腺素生成过多可能导致原发性肾上腺功能不全时出现的钠平衡改变和肾素释放。为了验证这一假设，对肾上腺切除的大鼠以及接受前列腺素抑制剂或替代地塞米松的动物进行了钠平衡和前列腺素生成的测量。与假手术对照组相比，肾上腺切除的大鼠两天钠平衡降低，血浆肾素浓度（PRC）、肾PGE2生成以及肾6-酮前列腺素F1α（6kPGF1α，PGI2的非酶代谢产物）升高；然而，未观察到主动脉6kPGF1α生成有明显变化。给肾上腺切除的大鼠注射地塞米松可使PRC恢复正常，但对钠平衡或前列腺素生成无影响。同样，前列腺素抑制剂也未改变肾上腺切除后的钠平衡或降低PRC。这些数据证实肾上腺切除的大鼠肾前列腺素生成增加，但表明这种升高并非直接由于糖皮质激素缺乏所致。此外，肾上腺功能不全时的PRC水平似乎并非由前列腺素介导。总之，肾前列腺素生成过多在肾上腺切除的大鼠中并不导致钠平衡改变或PRC升高。
