el-Beheiry H, Ruedy N, Wall R A, Murphy M, Wright J M
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver.
Can J Cardiol. 1993 Jan-Feb;9(1):41-6.
To investigate the acute and chronic effects of nitrendipine on plasma catecholamines in hypertensive patients.
The variations in level of plasma noradrenaline and adrenaline were measured in the supine and standing positions before and after the initial dose, and after 12 weeks of nitrendipine therapy. Following a washout placebo period, treatment was initiated by a single 20 mg dose of nitrendipine. This was followed by a double-blind randomization into two groups: one receiving 10 mg nitrendipine twice daily, the other receiving 20 mg once daily.
Clinical investigation unit, University Hospital (University of British Columbia site), Vancouver, British Columbia.
Sixteen patients (seven males and nine females), mean age 51 years (range 27 to 63), with mild to moderate, uncomplicated hypertension.
Two hours after administration of the initial 20 mg nitrendipine dose to all patients, there was a significant fall in the supine and standing systolic and diastolic blood pressure - from 164 +/- 3/102 +/- 1 to 139 +/- 2/87 +/- 2 mmHg, and from 153 +/- 4/105 +/- 1 to 139 +/- 3/90 +/- 1 mmHg, respectively. The supine and standing heart rates were unchanged. After 12 weeks of nitrendipine therapy, blood pressure was reduced (2 h after the dose) to a similar extent as that seen after the initial dose. Acute and chronic nitrendipine administration significantly increased supine and standing noradrenaline, but not adrenaline. Two hours after the initial 20 mg dose, supine noradrenaline increased from 3404 +/- 585 to 4005 +/- 644 pmol/L and standing noradrenaline increased from 3769 +/- 609 to 5821 +/- 615 pmol/L. At the end of the 12 weeks of therapy, similar dose-dependent effects were observed 2 h after the dose, but not 12 or 24 h after the dose, in both groups. The percentage increase in noradrenaline produced by nitrendipine in the standing position was consistently greater than in the supine position.
Chronic nitrendipine therapy results in a daily increase in plasma noradrenaline (2 h after the dose), and the effect is greater in the standing position.
研究尼群地平对高血压患者血浆儿茶酚胺的急性和慢性影响。
在初始剂量给药前及给药后、尼群地平治疗12周后，测量仰卧位和站立位时血浆去甲肾上腺素和肾上腺素水平的变化。经过一个洗脱安慰剂期后，以单次20mg剂量的尼群地平开始治疗。随后进行双盲随机分组，分为两组：一组每日两次服用10mg尼群地平，另一组每日一次服用20mg尼群地平。
不列颠哥伦比亚大学温哥华校区大学医院临床研究室。
16例患者（7例男性和9例女性），平均年龄51岁（范围27至63岁），患有轻度至中度、无并发症的高血压。
对所有患者给予初始20mg尼群地平剂量后两小时，仰卧位和站立位的收缩压和舒张压均显著下降——分别从164±3/102±1降至139±2/87±2mmHg，以及从153±4/105±1降至139±3/90±1mmHg。仰卧位和站立位的心率未改变。尼群地平治疗12周后，血压（给药后2小时）降低程度与初始剂量给药后相似。急性和慢性给予尼群地平均显著增加仰卧位和站立位的去甲肾上腺素，但不增加肾上腺素。给予初始20mg剂量后两小时，仰卧位去甲肾上腺素从3404±585增加至4005±644pmol/L，站立位去甲肾上腺素从3769±609增加至5821±615pmol/L。在治疗12周结束时，两组在给药后2小时观察到类似的剂量依赖性效应，但在给药后12小时或24小时未观察到。尼群地平在站立位引起的去甲肾上腺素增加百分比始终大于仰卧位。
慢性尼群地平治疗导致血浆去甲肾上腺素每日增加（给药后两小时），且在站立位时这种效应更大。
