Endocrine and vascular responses in hypertensive patients to long-term treatment with diltiazem.
Endocrine and vascular responses in hypertensive patients to long-term treatment with diltiazem.
复制标题
高血压患者对地尔硫卓长期治疗的内分泌和血管反应。
DOI：
10.1097/00005344-198704000-00002
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发表时间：
1987
影响因子：
3
通讯作者：
Swartz,SL
中科院分区：
文献类型：
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作者：
Swartz,SL
40例原发性高血压患者（年龄28-66岁）采用双盲、平行研究设计，随机接受地尔硫卓或氢氯噻嗪（HCTZ）治疗14周。HCTZ治疗的患者仰卧位体重显著降低（-6.0+/-1.5 lb; p< 0.001），脉搏增加（+ 6+/-2次/min; p< 0.001）。接受地尔硫卓治疗的患者体重没有变化，但脉搏明显下降（-5+/-2次/分; p< 0.05）。两个患者组仰卧位收缩压和舒张压的平均降低相当（HCTZ组为-16+/-4/-11+/-2 mmHg;地尔硫卓组为-17+/-3/-12+/-1 mmHg）。HCTZ和地尔硫卓治疗患者的血压降低不依赖于基线血浆肾素活性（PRA），但与PRA和前列腺素E2-代谢物（PGE 2-M）的变化显著相关（r= 0.51，p= 0.016）。HCTZ组PRA增加+2.8 +/-0.6 ng/ml/h（p< 0.001），地尔硫卓组PRA增加+0.8 +/-0.3 ng/ml/h（p< 0.05）。两种药物的PGE 2-M也升高（HCTZ为52+/-22 pg/ml;地尔硫卓为63+/-36 pg/ml）。因此，地尔硫卓和HCTZ是相似的，对每种药物的降压反应激活了肾素-血管紧张素系统，这反过来又伴随着PGE 2-M的产生增加。
Forty patients (aged 28-66 years) with essential hypertension were randomized to 14 weeks of treatment with diltiazem or hydrochlorothiazide (HCTZ) in a double-blind, parallel study design. A significant reduction in supine body weight (-6.0+/-1.5 lb; p< 0.001) and increase in pulse (+ 6+/-2 beats/min; p< 0.001) occurred in HCTZ-treated patients. Patients receiving diltiazem had no change in weight, but did have a significant fall in pulse (-5+/-2 beats/min; p< 0.05). The average reduction in supine systolic and diastolic blood pressures was comparable in both patient groups (-16+/-4/-11+/-2 mm Hg for HCTZ;-17+/-3/-12+/-1 for diltiazem). The reduction in blood pressure in HCTZ-and diltiazem-treated patients was not dependent on baseline plasma renin activity (PRA), but did correlate significantly with changes in PRA and prostaglandin E2-metabolite (PGE2-M)(r= 0.51, p= 0.016). PRA increased+ 2.8+/-0.6 ng/ml/h (p< 0.001) with HCTZ and+ 0.8+/-0.3 ng/ml/h (p< 0.05) with diltiazem. PGE2-M also rose with both drugs (52+/-22 pg/ml for HCTZ; 63+/-36 pg/ml for diltiazem). Thus, diltiazem and HCTZ were similar in that the depressor response to each drug activated the renin-angiotensin system, which in turn was accompanied by increased production of PGE2-M.