Effect of Prostaglandin Inhibition on the Hypertensive Action of Sodium‐Retaining Steroids
Effect of Prostaglandin Inhibition on the Hypertensive Action of Sodium‐Retaining Steroids
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前列腺素抑制对保钠类固醇高血压作用的影响
DOI：
10.1161/01.hyp.3.5.622
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发表时间：
1981
期刊：
影响因子：
8.3
通讯作者：
R. Horton
中科院分区：
文献类型：
--
作者：
K. Martin;R. Zipser;R. Horton
摘要 为了比较某些类固醇的钠潴留作用和对血压 (BP) 的影响，9 名无症状受试者每天两次（b.i.d.）给予氟氢可的松 0.3rag，5 名接受醋酸去氧皮质酮 (DOCA) 10ragIM b.i.d.，并将其与氟氢可的松或 DOCA 加前列腺素抑制 (PI) 或单独给予 PI 的效果进行比较。每 6 小时使用 50 mg 吲哚美辛或 400 mg 布洛芬完成 PI。所有患者每天接受 250 mEq Na+。单独使用氟氢可的松导致第 7 天时累积 Na + 平衡达到 305 ± 46 (SE) mEq，体重增加 2.5 ± 0.1 kg。到第 8 天，仰卧位和站立位的平均血压 (MAP) 均增加 9 ± 2 mm Hg。当氟氢可的松持续使用 16 天时，血压分别上升 14 ± 1 和 11 ± 1 mm Hg。 DOCA 造成类似的 Na+ 滞留，为 485 ± 125 mEq，体重增加 2 kg，并在第 7 天逃逸；然而，没有观察到血压变化。单独使用 PI 会导致 125 ± 49 mEq 滞留，体重增加 1 kg，并在第 4 天消失，但血压没有变化。相反，与单独使用氟氢可的松相比，第 9 天添加 PI 的氟氢可的松使仰卧位血压升高 21 ± 2 mm Hg (p < 0.01)，站立位血压升高 19 ± 2 mm Hg (p < 0.001)，但未观察到 Na + 或体重的更大变化。 DOCA 加 PI 也不会导致 Na + 保留或重量变化比单独使用 DOCA 更大；然而，血压从 86 ± 3 毫米汞柱增加到 98 ± 2 毫米汞柱 (p < 0.01)。所有研究组中均发现 PRA 和醛固酮受到类似的抑制。我们的结论是： 1）氟氢皮质酮对正常人具有升压作用，与其对钠平衡的影响无关； 2) DOCA 是一种纯盐皮质激素，服用数周后不会改变血压； 3) 正常人体内的PI会引起一定程度的钠潴留，但不会改变血压； 4) 前列腺素合成抑制剂增强氟氢可的松的升压作用，并升高 DOCA 治疗的人的血压，表明血管前列腺素在血压控制中发挥调节作用。
SUMMARY To compare the sodium-retaining action and the effect on blood pressure (BP) of certain steroids, nine nonnotensive subjects were given fludrocortisone0.3ragorally twice a day (b.i.d.), five received deoxycorticosterone acetate (DOCA) 10ragIM b.i.d., and this was compared to the effect of fludrocortisone or DOCA plus prostaglandin inhibition (PI) or PI given alone. PI was accomplished with either indomethacin 50 mg or ibuprofen 400 mg every 6 hours. All patients received 250 mEq Na+ daily. Fludrocortisone alone caused a cumulative Na + balance of 305 ± 46 (SE) mEq and weight gain 2.5 0.1 kg with escape by Day 7. Mean blood pressure (MAP) increased 9 ± 2 mm Hg in both supine and standing positions by Day 8. When fludrocortisone was continued for 16 days, BP rose 14 ± 1 and 11 ± 1 mm Hg respectively. DOCA caused similar Na+ retention of 485 ± 125 mEq, weight gain 2 kg, and escape by Day 7; however, no change in BP was observed. PI alone caused retention of 125 ± 49 mEq, weight gain 1 kg, and escape by Day 4, but no change in BP. In contrast, fludrocortisonewith PI added on Day 9 increased BP 21 ± 2 supine (p < 0.01) and 19 ± 2 mm Hg standing (p < 0.001) compared with fludrocortisone alone, but no greater change in Na + or weight was observed. DOCA plus PI also resulted in no greater Na + retention or change in weight than DOCA alone; however, BP increased from 86 ± 3 to 98 ± 2 mm Hg (p < 0.01). Similar suppression in PRA and aldosterone was noted in all of the study groups. We conclude that: 1)fludrocorticonehas a pressor action in normal humans Independent of its effect on sodium balance; 2) DOCA, a pure mineralocorticoid, does not alter BP when given for a period of weeks; 3) PI in normal humans causes some retention sodium, but does not alter BP; 4) prostaglandin synthesis inhibitors potentiate the pressor action offludrocortisoneand raise BP in DOCA-treated humans, suggesting that vascular prostaglandins play a modulating role in BP control.