Inomata Jun-ichiro, Murai Hisayoshi, Kaneko Shuichi, Hamaoka Takuto, Ikeda Tatsunori, Kobayashi Daisuke, Usui Soichiro, Furusho Hiroshi, Sugiyama Yu, Takata Shigeo, Takamura Masayuki
aDepartment of Disease Control and Homeostasis, Graduate School of Medical Science, Kanazawa University bKanazawa Municipal Hospital, Kanazawa, Japan *Hisayoshi Murai and Shuichi Kaneko contributed equally to this article.
J Hypertens. 2014 Sep;32(9):1898-904. doi: 10.1097/HJH.0000000000000270.
Calcium channel blockers (CCBs) are used as antihypertensive agents and have a strong vasodilatory effect; however, the sympathetic activation mediated by baroreflex might cause adverse effects. A recently developed CCB, azelnidipine, decreases the heart rate (HR) while lowering blood pressure (BP), possibly by inhibiting sympathetic nerve activity in animal models. In this study, we evaluated whether azelnidipine inhibited sympathetic nerve activity, compared to amlodipine, in primary hypertensive patients.
We conducted a prospective, randomized, open-label, and crossover study of 14 patients. We measured the patients' BP, HR and baroreflex sensitivity, and directly recorded muscle sympathetic nerve activity (MSNA), via microneurography, after treatment with either CCB for 8 weeks.
Although systolic and diastolic BPs did not differ between the azelnidipine and amlodipine groups, the HR in the azelnidipine group significantly decreased compared with that in the amlodipine group. MSNA was significantly reduced in the azelnidipine compared with the amlodipine group (47.7 ± 14.9 vs. 61.5 ± 10.7 bursts per 100 beats, P < 0.05). However, no significant difference was observed in terms of the baroreflex control of HR, or MSNA, between the two groups.
Our data show, first, that azelnidipine, compared with amlodipine, exerted a favorable effect on sympathetic nerve activity, without affecting baroreflex sensitivity, in hypertensive patients. These results indicate that azelnidipine might be useful for treating hypertensive patients, in whom hypertension is complicated by heart failure and ischemic heart disease.
钙通道阻滞剂(CCB)被用作抗高血压药物,具有强大的血管舒张作用;然而,压力反射介导的交感神经激活可能会导致不良反应。最近开发的一种CCB——阿折地平,在降低血压(BP)的同时可降低心率(HR),在动物模型中可能是通过抑制交感神经活动实现的。在本研究中,我们评估了在原发性高血压患者中,与氨氯地平相比,阿折地平是否能抑制交感神经活动。
我们对14例患者进行了一项前瞻性、随机、开放标签的交叉研究。在用两种CCB治疗8周后,我们测量了患者的血压、心率和压力反射敏感性,并通过微神经ography直接记录肌肉交感神经活动(MSNA)。
尽管阿折地平组和氨氯地平组的收缩压和舒张压没有差异,但阿折地平组的心率与氨氯地平组相比显著降低。与氨氯地平组相比,阿折地平组的MSNA显著降低(每100次心跳47.7±14.9次与61.5±10.7次爆发,P<0.05)。然而,两组在心率的压力反射控制或MSNA方面未观察到显著差异。
我们的数据首先表明,在高血压患者中,与氨氯地平相比,阿折地平对交感神经活动有良好影响,且不影响压力反射敏感性。这些结果表明,阿折地平可能对治疗合并心力衰竭和缺血性心脏病的高血压患者有用。