Pancera P, Presciuttini B, Sansone S, Montagna L, Paluani F, Covi G, Lechi A
University of Verona, Italy.
J Hypertens. 1999 Apr;17(4):513-21. doi: 10.1097/00004872-199917040-00009.
To define the changes in variability of heart rate and of blood pressure during vasodilation in a group of hypertensive patients treated with an angiotensin II type I (AT1) receptor inhibitor.
Losartan (50 mg/day at 0800 h) or placebo were administered for 3 weeks according to a single blind, crossover, randomized protocol, to 18 hypertensive patients (16 men and two women, mean age 42 + 3.6 years). Continuous ECG recording and beat-to-beat blood pressure monitoring were carried out with subjects in the supine position and during a head-up tilt test, as well as after sublingual administration of trinitroglycerine. The elaboration of ECG traces in the frequency domain, was carried out using an autoregressive method and measured using the autoregressive moving average technique.
Orthostatic stimulus, both during treatment with losartan and with placebo, caused a significant decrease in the heart rate high frequency power; on the other hand, the low frequency power appeared unchanged after placebo and was significantly reduced with losartan. Five minutes after the administration of trinitroglycerine, the low frequency power with placebo showed a significant increase (817 -+ 221 versus 465 + 101 ms2, P < 0.03). No change was recorded in total power nor in low frequency or high frequency power during losartan therapy. The ratio of low frequency to high frequency powers showed a sympathetic prevalence during vasodilation only during placebo treatment, whereas a mainly unchanged balance was maintained during losartan treatment Blood pressure variability showed a sympathetic prevalence after upright and trinitroglycerine stimulation only in placebo-treated subjects.
Our study demonstrated that vasodilation is not able to evoke an unbalancing of the autonomic modulation in hypertensive patients treated with an AT1 receptor inhibitor, but permits the maintenance of a significant vagal component, thus highlighting the favorable profile of this drug in the autonomic control of circulation.
确定一组接受血管紧张素II 1型(AT1)受体抑制剂治疗的高血压患者在血管舒张过程中心率和血压变异性的变化。
按照单盲、交叉、随机方案,对18例高血压患者(16例男性和2例女性,平均年龄42±3.6岁)给予氯沙坦(每日50毫克,上午8点服用)或安慰剂,为期3周。在受试者仰卧位、进行头高位倾斜试验时以及舌下含服硝酸甘油后,进行连续心电图记录和逐搏血压监测。使用自回归方法在频域对心电图轨迹进行分析,并采用自回归移动平均技术进行测量。
在氯沙坦和安慰剂治疗期间,直立刺激均导致心率高频功率显著降低;另一方面,安慰剂治疗后低频功率未变,而氯沙坦治疗后低频功率显著降低。服用硝酸甘油5分钟后,安慰剂组的低频功率显著增加(817±221对465±101毫秒²,P<0.03)。氯沙坦治疗期间,总功率、低频功率或高频功率均无变化。仅在安慰剂治疗期间血管舒张时低频与高频功率之比显示交感神经占优势,而氯沙坦治疗期间维持主要未变的平衡。仅在接受安慰剂治疗的受试者中,直立和硝酸甘油刺激后血压变异性显示交感神经占优势。
我们的研究表明,血管舒张不会引起接受AT1受体抑制剂治疗的高血压患者自主调节失衡,而是允许维持显著的迷走神经成分,从而突出了该药物在自主循环控制方面的有利特征。