Säynävälammi P, Pörsti I, Pörsti P, Nurmi A K, Seppälä E, Manninen V, Vapaatalo H
Department of Biomedical Sciences, University of Tampere, Finland.
J Cardiovasc Pharmacol. 1988 Jul;12(1):88-93. doi: 10.1097/00005344-198807000-00012.
Fourteen patients with mild to moderate essential hypertension were randomized, after a baseline placebo period of 4 weeks, to receive the angiotensin converting enzyme (ACE) inhibitor quinapril or a placebo. During a 12 week, double-blind phase, the dosage of quinapril was increased from 10 to 40 mg twice daily being doubled every 4 weeks. At the end of the baseline period and of each month of the double-blind phase, 12 h overnight urine collections were made and morning blood samples were taken about 12 h after the last dose of medication. During the double-blind phase, blood pressure in the quinapril group (n = 7) decreased from 159 +/- 3/105 +/- 1 to 141 +/- 6/94 +/- 2 mm Hg (mean +/- SEM). Serum ACE activity and plasma angiotensin II concentration were reduced to 4 +/- 1% and 14 +/- 1% of the pretreatment values, respectively. Neither the plasma concentrations nor the urinary excretions of prostaglandin E2, 6-keto-prostaglandin F1 alpha (a prostacyclin metabolite), or thromboxane B2 (a metabolite of thromboxane A2) were affected by quinapril. In the placebo group, blood pressure tended to decline but the biochemical variables remained essentially unchanged. These results indicate that prostanoids are not involved in the antihypertensive action of quinapril, the principal effect of which seems to be inhibition of the renin-angiotensin system.
14例轻度至中度原发性高血压患者在经过4周的基线安慰剂期后，被随机分组，分别接受血管紧张素转换酶（ACE）抑制剂喹那普利或安慰剂治疗。在为期12周的双盲阶段，喹那普利的剂量从每日两次，每次10毫克增加到40毫克，每4周翻倍一次。在基线期结束时以及双盲阶段的每个月末，收集12小时夜间尿液，并在最后一剂药物服用约12小时后采集早晨血样。在双盲阶段，喹那普利组（n = 7）的血压从159 +/- 3/105 +/- 1毫米汞柱降至141 +/- 6/94 +/- 2毫米汞柱（均值 +/- 标准误）。血清ACE活性和血浆血管紧张素II浓度分别降至治疗前值的4 +/- 1%和14 +/- 1%。喹那普利对前列腺素E2、6-酮-前列腺素F1α（一种前列环素代谢产物）或血栓素B2（血栓素A2的一种代谢产物）的血浆浓度和尿排泄均无影响。在安慰剂组，血压有下降趋势，但生化指标基本保持不变。这些结果表明，前列腺素类物质不参与喹那普利的降压作用，其主要作用似乎是抑制肾素-血管紧张素系统。
