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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Effects of amlodipine and cilnidipine on cardiac sympathetic nervous system and neurohormonal status in essential hypertension.
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Effects of amlodipine and cilnidipine on cardiac sympathetic nervous system and neurohormonal status in essential hypertension.

机译:氨氯地平和西尼地平对原发性高血压心脏交感神经系统和神经激素状态的影响。

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N-Type calcium channel antagonists may suppress sympathetic activity. The purpose of this study was to assess the effects of amlodipine and cilnidipine on the cardiac sympathetic nervous system and the neurohormonal status of essential hypertension. 123I-metaiodobenzylguanidine (MIBG) cardiac imaging was performed and blood samples were taken to determine plasma renin activity and plasma norepinephrine concentration before and 3 months after drug administration in 47 patients with mild essential hypertension. Twenty-four of the patients were treated with 5 to 10 mg/d of amlodipine; the other 23 were treated with 10 to 20 mg/d of cilnidipine. For comparison, 12 normotensive subjects were also studied. No significant differences were found in the basal characteristics between the 2 hypertensive groups. In both hypertensive groups, both the systolic and diastolic blood pressures were significantly reduced to similar levels 3 months after drug treatment. Before the drug treatment, the 2 hypertensive groups had a significantly higher washout rate and lower heart-to-mediastinum (H/M) ratio compared with the normotensive subjects. The H/M ratio significantly increased (P<0.05) in combination with a decreased washout rate (P<0.02) after drug treatment in the cilnidipine group. In the amlodipine group, a significant decrease in washout rate (P<0. 04) was noted, without an increase in the H/M ratio. However, no significant changes were found in plasma renin activity and plasma norepinephrine concentration in either group. Thus, in patients with essential hypertension, cilnidipine suppressed cardiac sympathetic overactivity and amlodipine had a little suppressive effect. Cilnidipine may provide a new strategy for treatment of cardiovascular diseases with sympathetic overactivity.
机译:N型钙通道拮抗剂可能会抑制交感神经活动。这项研究的目的是评估氨氯地平和西尼地平对心脏交感神经系统和原发性高血压的神经激素状态的影响。对47例轻度原发性高血压患者进行123I-甲酰氨基苄基胍(MIBG)心脏成像,并抽取血样测定血浆肾素活性和血浆去甲肾上腺素浓度。 24例患者接受了5-10 mg / d的氨氯地平治疗;其余23种分别以10至20 mg / d的西尼地平治疗。为了比较,还研究了12名血压正常的受试者。两组高血压患者的基础特征无明显差异。在两个高血压组中,药物治疗后3个月,收缩压和舒张压均显着降低至相似水平。与正常血压受试者相比,在药物治疗之前,这两个高血压组的冲洗率显着较高,而心脏与纵隔(H / M)的比例较低。西尼地平组药物治疗后,H / M比显着增加(P <0.05),同时洗脱率降低(P <0.02)。在氨氯地平组中,洗脱率显着下降(P <0。04),而H / M比没有增加。然而,两组中血浆肾素活性和血浆去甲肾上腺素浓度均未见明显变化。因此,在患有原发性高血压的患者中,西尼地平抑制心脏交感神经过度活动,而氨氯地平具有少许抑制作用。西尼地平可能为治疗交感神经过度活跃的心血管疾病提供新的策略。

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