ROLE OF NO GENERATION IN BETA-ADRENOCEPTOR-MEDIATED STIMULATION OF RABBIT AIRWAY CILIARY MOTILITY

To determine possible contribution of nitric oxide (NO) to the stimula tory action of P-adrenoceptor agonist on ciliary motility; we measured ciliary beat frequency (CBF) of rabbit cultured tracheal epithelial c ells by photoelectric method and NO release by specific amperometric s ensors for this molecule in vitro. Salbutamol increased CBF, an effect that was potentiated by superoxide dismutase. Pretreatment of cells v ith N-G-nitro-L-arginine methyl ester (L-NAME) attenuated the salbutam ol-induced increase in CBF, causing a rightward displacement of the co ncentration-response curve by 2-2.5 log units, whereas N-G-nitro-D-arg inine methyl ester had no effect. The inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Immersion of the NO-sele ctive electrode in the medium containing epithelial cells detected bas eline current of 4.6-14.5 pA, which was abolished by L-NAME. Salbutamo l dose-dependently increased the concentration of NO in the medium, th e maximal increase being 56.2 +/- 5.3 nM (mean +/- SE; P < 0.001). The se results suggest that NO is spontaneously released by airway epithel ium and that the enhanced release of this molecule may play a role in the beta-adrenoceptor-mediated stimulation of ciliary motility.