['Complex mechanisms regulate nitric oxide (NO) synthesis. Cigarette smoking decreases fractional exhaled NO (FE(NO)), while asthmatic inflammation increases FE(NO). To assess whether the smoking-induced decrease in FE(NO) levels was reversible, asthmatic and non-asthmatic smokers inhaled the NO synthase (NOS) substrate, L-arginine. Aminoguanidine, a relatively selective Type II NOS inhibitor, was used also to assess the role of NOS subtypes in these changes of FE(NO).', 'The study was a single-blinded, placebo-controlled, cross-over design in two parts. Part I: smoking asthmatic and non-asthmatic smoking subjects smoked one cigarette and then inhaled nebulised L-arginine or L-alanine (control). Spirometry, FE(NO), nasal NO (FN(NO)), FE(CO), were measured for 4 h. Part II: subjects inhaled nebulised aminoguanidine prior to an identical protocol as in Part I. Change in FE(NO) was assessed as area under the curve (AUC).', 'Part I: In asthmatic smokers, cigarette smoking followed by L-arginine caused a significant median increase in AUC of 29.2(17)% FE(NO) change/hour (p = 0.04), which did not occur in non-asthmatic smokers (baseline FE(NO) 12.7(7.1-18) vs. 6.7(4-9.2) ppb, respectively). Part II: Aminoguanidine prior to smoking caused a significant fall in FE(NO) in both asthmatic and non-asthmatic smokers. L-arginine showed significant reversal of this effect in both asthmatic and non-asthmatic subjects.'] Does l-arginine reverse cigarette-induced reduction of fractional exhaled nitric oxide in asthmatic smokers?