Honda M, Izumi Y, Hatano M
2nd Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Nihon Naibunpi Gakkai Zasshi. 1988 Jan 20;64(1):31-8. doi: 10.1507/endocrine1927.64.1_31.
Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.
为了研究前列腺素E2（PGE2）和激肽的尿排泄情况，将螺内酯给予自发性高血压大鼠（SHR）。13只SHR被分为2组，其中一组（螺内酯未治疗组）（n = 6）皮下注射0.1 ml芝麻油，另一组（螺内酯治疗组）（n = 7）皮下注射0.1 ml芝麻油溶解的20 mg螺内酯，连续给药10天，随后测定体重、血压、尿量以及24小时尿中Na、K、激肽和PGE2的排泄水平。在这些动物断头处死以测定血浆肾素活性（PRA）后采集血样。结果显示，螺内酯治疗组血压降低，尿Na排泄增加。另一方面，给予螺内酯后，24小时尿中PGE2排泄水平立即显著降低（p < 0.05），并在实验结束前一直维持在较低水平。然而，螺内酯治疗组和未治疗组24小时尿激肽水平变化相似，两组间无显著差异。这些结果表明，螺内酯对尿PGE2排泄有抑制作用，其作用并非通过肾脏中激肽的产生介导，而是由螺内酯自身的直接作用产生。
