Amlodipine increases nitric oxide production in exhaled air during exercise in patients with essential hypertension
Amlodipine increases nitric oxide production in exhaled air during exercise in patients with essential hypertension
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DOI：
10.1016/j.amjhyper.2004.05.025
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发表时间：
2004-09-01
影响因子：
3.2
通讯作者：
Nagai, R
中科院分区：
文献类型：
--
作者：
Kato, M;Matsumoto, A;Nagai, R
背景：原发性高血压患者内皮细胞产生的一氧化氮 (NO) 减弱。我们研究了氨氯地平治疗是否会增加原发性高血压患者在休息和运动时的呼出一氧化氮输出量 (VNO)。方法：我们研究了氨氯地平对 7 名未经治疗的高血压患者的作用。在氨氯地平治疗 2 个月之前和之后，对这些患者进行心肺运动测试和呼出气体 NO 测量。结果：氨氯地平降低了静息和运动期间的血压 (BP)（静息时：147.1 +/- 6.4 [SEM]/89.9 +/- 4.4 v 133.6 +/- 5.4/82.7 +/- 3.9 mm Hg，P < .05；峰值运动时：224.9 +/- 8.0/113.1 +/- 5.3 v 207.0 +/- 6.0/100.7 +/- 5.0 mm Hg，P < .05），不影响心率（休息时：67.6 +/- 3.9 v 70.4 +/- 4.5 次/分钟，P = .33；峰值运动时：146.4 +/- 7.4 v 144.0 +/- 7.2 次/分钟，P = .49）。氨氯地平不会影响休息或运动时的每分钟通气量 (VE)。它不会改变无氧阈值、峰值摄氧量（峰值 VO2）或峰值工作负荷。然而，氨氯地平治疗后，静息状态下的 VNO 显着升高 (130.8 +/- 19.4 v 180.4 +/- 24.8 nL/min，P < .05) 和运动高峰时 (380.0 +/- 47.5 v 582.6 +/- 74.3 nL/min，P < .05)。结论：氨氯地平增加了 NO 的产生，至少在肺部原发性高血压患者的循环。除了其抗高血压作用外，氨氯地平在其他器官的脉管系统中增强一氧化氮的产生可能有助于其对心血管系统的有益作用。 (C) 2004 年美国高血压杂志有限公司。
Background: Endothelial production of nitric oxide (NO) is attenuated in patients with essential hypertension. We investigated whether treatment with amlodipine increased exhaled NO output (VNO) at rest and during exercise in patients with essential hypertension.Methods: We studied the effect of amlodipine in seven untreated hypertensive patients. Cardiopulmonary exercise testing and NO measurement of exhaled air were performed on these patients before and after 2 months of amlodipine treatment.Results: Amlodipine decreased blood pressure (BP) both at rest and during exercise (at rest: 147.1 +/- 6.4 [SEM]/89.9 +/- 4.4 v 133.6 +/- 5.4/82.7 +/- 3.9 mm Hg, P < .05; at peak exercise: 224.9 +/- 8.0/113.1 +/- 5.3 v 207.0 +/- 6.0/100.7 +/- 5.0 mm Hg, P < .05) without affecting heart rate (at rest: 67.6 +/- 3.9 v 70.4 +/- 4.5 beats/min, P = .33; peak exercise: 146.4 +/- 7.4 v 144.0 +/- 7.2 beats/min, P = .49). Amlodipine did not affect minute ventilation (VE) at rest or during exercise. It did not alter anaerobic threshold, peak oxygen uptake (peak VO2), or peak workload. However, after amlodipine treatment, VNO was significantly greater both at rest (130.8 +/- 19.4 v 180.4 +/- 24.8 nL/min, P < .05) and at peak exercise (380.0 +/- 47.5 v 582.6 +/- 74.3 nL/min, P < .05).Conclusions: Amlodipine increased NO production, at least in the pulmonary circulation, in patients with essential hypertension. In addition to its antihypertensive effect, the enhancement of NO production by amlodipine in the vasculature of other organs may contribute to its beneficial effects on the cardiovascular system. (C) 2004 American Journal of Hypertension, Ltd.