Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 170, Issue 2, Pages 148-153Publisher
AMER THORACIC SOC
DOI: 10.1164/rccm.200309-1304OC
Keywords
asthmatic; L-arginine; amino acids; nitric oxide; nitric oxide synthase
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Funding
- NCRR NIH HHS [M01 RR001271, M01-RR01271] Funding Source: Medline
- NHLBI NIH HHS [K23 HL004386, HL-04386-03, HL-20985, R01 HL066355, HL-66355] Funding Source: Medline
- NIGMS NIH HHS [GM57384, R01 GM057384] Funding Source: Medline
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Recent studies suggest that a nitric oxide (NO) deficiency and elevated arginase activity may play a role in the pathogenesis of asthma. Although much attention has been directed toward measurements of exhaled NO in asthma, no studies to date have evaluated levels of plasma arginase or arginine, the substrate for NO production, in patients with asthma. This study, therefore, measured amino acid levels, arginase activity, and nitric oxide metabolites in the blood of patients with asthma, as well as NO in exhaled breath. Although levels of virtually all amino acids were reduced, patients with asthma exhibited a striking reduction in plasma arginine levels compared with normal control subjects without asthma (45 +/- 22 vs. 94 +/- 29 muM, p < 0.0001), and serum arginase activity was elevated (1.6 +/- 0.8 vs. 0.5 +/- 0.3 mumol/ml/hour, asthma vs. control, p < 0.0001). High arginase activity in patients with asthma may contribute to low circulating arginine levels, thereby limiting arginine bioavailability and creating a NO deficiency that induces hyperreactive airways. Addressing the alterations in arginine metabolism may result in new strategies for treatment of asthma.
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