Amlodipine increases nitric oxide production in exhaled air during exercise in patients with essential hypertension

Background Endothelial production of nitric oxide (NO) is attenuated in patients with essential hypertension. We investigated whether treatment with amlodipine increased exhaled NO output (V̇NO) 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 (V̇E) at rest or during exercise. It did not alter anaerobic threshold, peak oxygen uptake (peak V̇O2), or peak workload. However, after amlodipine treatment, V̇NO 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.