J. Tamaoki et al., ROLE OF NO GENERATION IN BETA-ADRENOCEPTOR-MEDIATED STIMULATION OF RABBIT AIRWAY CILIARY MOTILITY, American journal of physiology. Cell physiology, 37(6), 1995, pp. 1342-1347
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.