BACKGROUND: -adrenergic response. Airway GSNO levels are often low in asthma. OBJECTIVE: We studied the effects of inhaled GSNO (iGSNO) in human asthma. METHODS: -adrenergic agonist response and fractional exhaled nitric oxide, and expression of GSNO metabolic genes from bronchoscopic biopsy samples using spatial transcriptomics. RESULTS: -adrenergic receptor response; the magnitude of increase was related, and additive, to the receptor response (P < .001). SCoR2 (AKR1A1 gene), encoding a GSNO degrading enzyme, was upregulated in airway epithelium, and higher SCoR2 expression was associated with reduced iGSNO bronchodilation. Sustained elevation in fractional exhaled nitric oxide after iGSNO, indicating reduced GSNO catabolism, was a biomarker for iGSNO effect. CONCLUSION: -adrenergic receptor agonist benefit.
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Gaston et al. (2026) studied this question.
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