Pedrinelli R, Magagna A, Abdel-Haq B, Salvetti A
Adv Prostaglandin Thromboxane Leukot Res. 1985;13:147-50.
The finding that sulindac, in contrast to indomethacin, does not inhibit renal prostaglandins (PGs) can offer the means to study the role of systemic and/or renal PGs in the control of renin. Therefore we studied, using a randomized cross-over design, the influence of treatment with sulindac and indomethacin on plasma renin activity (PRA) of essential hypertensive patients, which was measured either after standing or after chronic captopril and chlorthalidone administration. In the captopril-treated group, serum thromboxane B2 (TXB2) and urinary 6-keto-PGF1alpha were significantly reduced by indomethacin, while sulindac reduced only serum TXB2. PRA was significantly reduced by indomethacin in the three groups and by sulindac only in standing and captopril-treated patients. These findings suggest that systemic PGs are mainly involved in the control of renin during standing and angiotensin-converting enzyme (ACE) inhibition, while mainly renal PGs play a role in the control of renin during chronic thiazide-like diuretic administration.
与吲哚美辛不同，舒林酸不抑制肾前列腺素（PGs），这一发现为研究全身和/或肾PGs在肾素控制中的作用提供了手段。因此，我们采用随机交叉设计，研究了舒林酸和吲哚美辛治疗对原发性高血压患者血浆肾素活性（PRA）的影响，分别在站立后或长期服用卡托普利和氢氯噻嗪后测量PRA。在卡托普利治疗组中，吲哚美辛显著降低血清血栓素B2（TXB2）和尿6-酮-PGF1α，而舒林酸仅降低血清TXB2。吲哚美辛在三组中均显著降低PRA，舒林酸仅在站立和卡托普利治疗的患者中降低PRA。这些发现表明，全身PGs在站立和血管紧张素转换酶（ACE）抑制期间主要参与肾素的控制，而主要是肾PGs在长期噻嗪类利尿剂给药期间对肾素的控制中起作用。
