Minuz P, Lechi A, Arosio E, Degan M, Capuzzo M G, Lechi C, Corsato M, Dalla Riva A, Velo G P
Clinica Medica, University of Verona, Policlinico Borgo Roma, Italy.
J Clin Hypertens. 1987 Dec;3(4):645-53.
It has been suggested that angiotensin-converting enzyme (ACE) inhibitors may also act through the renal prostaglandin (PG) system; moreover, it has been shown that nonsteroidal antiinflammatory drugs (NSAIDs) are capable of reducing the antihypertensive activity of ACE inhibitors. Sixteen essential hypertensive patients (WHO stages, I-II, eight on a low-sodium diet and eight on a high-sodium diet) were treated with enalapril, 20 mg/day per os, for 4 days. On days 3 and 4, ibuprofen, 1,200 mg/day per os, was also given. Enalapril reduced blood pressure, particularly in the group on the low-sodium diet. Urinary 6-keto-PGF1 alpha, an indicator of renal PGI2 production (determined by HPLC-RIA), increased in the first few hours after enalapril in the low-sodium group. Ibuprofen did not reduce the antihypertensive effect of enalapril, nor did it affect plasma renin activity or plasma aldosterone. Only a slight reduction in 6-keto-PGF1 alpha excretion was observed after enalapril plus ibuprofen. It is suggested that the effect of enalapril on urinary 6-keto-PGF1 alpha excretion is largely dependent on factors such as sodium intake.
有人提出血管紧张素转换酶（ACE）抑制剂可能也通过肾脏前列腺素（PG）系统发挥作用；此外，已有研究表明非甾体抗炎药（NSAIDs）能够降低ACE抑制剂的降压活性。16例原发性高血压患者（世界卫生组织分期为I-II期，8例采用低钠饮食，8例采用高钠饮食）口服依那普利，每日20mg，共治疗4天。在第3天和第4天，还口服布洛芬，每日1200mg。依那普利降低了血压，尤其是在低钠饮食组。尿6-酮-PGF1α是肾脏PGI2生成的一个指标（通过高效液相色谱-放射免疫分析法测定），在低钠组服用依那普利后的最初几个小时内升高。布洛芬并未降低依那普利的降压效果，也未影响血浆肾素活性或血浆醛固酮。依那普利加布洛芬后仅观察到6-酮-PGF1α排泄略有减少。提示依那普利对尿6-酮-PGF1α排泄的影响在很大程度上取决于钠摄入量等因素。
