Clinical studies have shown that oxidizing substances like hydrogen peroxide (H2O2) and ammonium persulfate used in the hair cosmetic industry may cause airway diseases. In in vitro experiments with isolated guinea pig tracheae ammonium persulfate solutions induced an initial transient relaxation of smooth muscles. This relaxation could be measured by a decrease in isometric pressure in the cannulated trachea instilled with ammonium persulfate at a hydrostatic pressure of 2.5 kPa. In control experiments, saline caused an initial pressure decrease of less than 10% within one minute. In contrast, instillation of different ammonium persulfate solutions (9.10(-5) to 9.10(-2) M) effectively dilated tracheae and resulted in a concentration-dependent drop in intratracheal pressure to 1.53 +/- 0.62 kPa (61% of the instillation pressure). The effect of ammonium persulfate on smooth muscles is obviously mediated by nitric oxide because the relaxation could be blocked by inhibitors of nitric oxide synthase (L-NMMA 40 microM and L-NAME 200 microM). The precursor of nitric oxide, L-arginine (1 mM), the D-isomers of the inhibitors and a mixture of L-arginine and L-NAME did not affect the ammonium persulfate-induced initial intratracheal pressure decrease. The results allow us to conclude that acutely elicited tracheal muscle dilatation by ammonium persulfate is mediated by nitric oxide. However, it is possible that a continuous use of oxidizing substances may lead to epithelial damage and, therefore, reduce the production of nitric oxide, thus facilitating constrictory responses.