Calcium-channel blockade with nifedipine and angiotensin converting-enzyme inhibition with captopril in the therapy of patients with severe primary hypertension.

Calcium-channel blockade with nifedipine and angiotensin converting-enzyme inhibition with captopril in the therapy of patients with severe primary hypertension.
复制标题

硝苯地平钙通道阻断和卡托普利血管紧张素转换酶抑制治疗严重原发性高血压患者。

DOI:
10.1161/01.cir.70.2.279
复制
发表时间:
1984
期刊:
影响因子:
37.8
通讯作者:
A. Bartorelli
A. Bartorelli
中科院分区:
医学1区
文献类型:
--
作者:
M. Guazzi;N. D. De Cesare;C. Galli;A. Salvioni;C. Tramontana;G. Tamborini;A. Bartorelli

文献摘要

被引文献

相似文献

硝苯地平(10 mg,qd)和卡托普利(25 mg,qd)对14例重度高血压病患者进行单独和联合治疗。每个研究周期为1周。循环反应通过每小时压力和脉率读数进行评估。口服硝苯地平后,血压下降在1小时或更短时间内最大,通常伴有心悸和脉搏加快;对于每6小时给药的方案,每次给药后血压有恢复的趋势,下一次给药中断,因此在整个24小时内血压仍显著下降,尽管压力波动明显。卡托普利降压作用的迅速程度相似,但降压幅度和持续时间不那么明显。当转换酶抑制剂与钙通道阻滞剂联合使用时,血压波动不会被消除,但降压反应肯定会增强,从而使正常血压在白天维持几个小时。卡托普利的其他积极作用是减缓心率反应,防止硝苯地平引起的脚踝凹陷或浮肿。卡托普利促进小动脉和小静脉扩张的平衡是这些效应的可能机制。两药合用后,左心功能未见下降,甚至可能有所改善;血尿素氮、血清电解质、肌酐浓度无明显变化。血浆肾素活性随卡托普利升高,加入硝苯地平后恢复至基线水平,提示钙通道阻滞剂对肾素释放有干扰作用。
Nifedipine (10 mg qid) and captopril (25 mg qid) were tested alone and in combination in 14 patients suffering from severe primary hypertension. Each study period was of 1 week's duration. Circulatory response was evaluated through hourly pressure and pulse rate readings. The fall in pressure after oral nifedipine was maximal within 1 hr or less and was generally accompanied by palpitation and increase in pulse rate; with a six hourly dosing regimen the tendency of blood pressure to recover after each dose was interrupted by the next dose, so that values remained significantly reduced throughout the 24 hr, although pressure fluctuations were evident. Promptness of the antihypertensive action of captopril was similar, but the magnitude and the duration of the fall in pressure were less pronounced. When the converting-enzyme inhibitor was combined with the calcium-channel blocker, pressure fluctuations were not abolished, but the antihypertensive response was definitely enhanced, so that normal blood pressure was maintained for several hours during the day. Additional positive effects of captopril were mitigation of the heart rate reaction and prevention of the ankle pitting or edema elicited by nifedipine. A balance in arteriolar and venular dilatation promoted by captopril is the suggested mechanism for these effects. With the two-drug combination the function of the left ventricle was not reduced and possibly improved; blood urea nitrogen and serum electrolyte and creatinine concentration were not affected. Plasma renin activity increased with captopril and reverted toward baseline with the addition of nifedipine, suggesting an interference of the calcium-channel blocker with the release of renin.