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J Appl Physiol 90: 586-592, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 2, 586-592, February 2001

Role of nitric oxide in the airway response to exercise in healthy and asthmatic subjects

H. W. F. M. De Gouw1, S. J. Marshall-Partridge2, H. Van der Veen1, J. G. Van den Aardweg1, P. S. Hiemstra1, and P. J. Sterk1

Departments of 1 Pulmonology and 2 Clinical Pharmacy and Toxicology, Leiden University Medical Center, NL-2300 RC Leiden, The Netherlands

A role of nitric oxide (NO) has been suggested in the airway response to exercise. However, it is unclear whether NO may act as a protective or a stimulatory factor. Therefore, we examined the role of NO in the airway response to exercise by using N-monomethyl-L-arginine (L-NMMA, an NO synthase inhibitor), L-arginine (the NO synthase substrate), or placebo as pretreatment to exercise challenge in 12 healthy nonsmoking, nonatopic subjects and 12 nonsmoking, atopic asthmatic patients in a double-blind, crossover study. Fifteen minutes after inhalation of L-NMMA (10 mg), L-arginine (375 mg), or placebo, standardized bicycle ergometry was performed for 6 min using dry air, while ventilation was kept constant. The forced expiratory volume in 1-s response was expressed as area under the time-response curve (AUC) over 30 min. In healthy subjects, there was no significant change in AUC between L-NMMA and placebo treatment [28.6 ± 17.0 and 1.3 ± 20.4 (SE) for placebo and L-NMMA, respectively, P = 0.2]. In the asthmatic group, L-NMMA and L-arginine induced significant changes in exhaled NO (P < 0.01) but had no significant effect on AUC compared with placebo (geometric mean ± SE: -204.3 ± 1.5, -186.9 ± 1.4, and -318.1 ± 1.2% · h for placebo, L-NMMA, and L-arginine, respectively, P > 0.2). However, there was a borderline significant difference in AUC between L-NMMA and L-arginine treatment (P = 0.052). We conclude that modulation of NO synthesis has no effect on the airway response to exercise in healthy subjects but that NO synthesis inhibition slightly attenuates exercise-induced bronchoconstriction compared with NO synthase substrate supplementation in asthma. These data suggest that the net effect of endogenous NO is not inhibitory during exercise-induced bronchoconstriction in asthma.

exercise-induced bronchoconstriction; vascular leakage; exhaled nitric oxide


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