[Nitric-oxidergic mechanisms in the regulation of the bronchi and their significance in the pathogenesis of bronchial asthma].

AIM

Assessment of NO-synthase (NOS) activity in bronchial asthma (BA) basing on cytochemical identification and quantitation of NADPN-diaphorase.

MATERIALS AND METHODS

Operative samples from 12 BA patients and biopsies from 8 patients free of bronchial inflammation or obstruction. Experimental data on control and BA rat males injected either with NOS agonist acetyl choline (AC) or beta-2-agonist fenoterol (F).

RESULTS

A direct relationship was found between BA severity and activity of NADPN-diaphorase resultant from activation of inducible NOS (iNOS) mediating constrictive effect via different cellular and humoral mechanisms. AC treatment caused bronchial relaxation and severe constriction in control and BA rats, respectively, though NADPN-diaphorase activity was enhanced in both groups. Introduction of F brought about bronchial relaxation in both groups. However, there were some cases of constriction in the bronchi with impaired epithelium and high baseline iNOS activity.

CONCLUSION

In intact bronchial epithelium, administration of cholino- and adrenoreceptors agonists induced bronchial myocyte relaxation due to activation of constitutive NOS. In impaired bronchial epithelium, AC stimulates iNOS induction provoking severe constriction of small bronchi.