Role of nitric oxide generation in [beta]-adrenoceptor-mediated
stimulation of rabbit airway ciliary motility.
Tamaoki, Jun, Atsushi Chiyotani, Mitsuko Kondo, and Kimio Konno.
First Department of Medicine, Tokyo Women's Medical College, Tokyo
162, Japan
APStracts 2:0118C, 1995.
To determine possible contribution of nitric oxide (NO) to the
stimulatory action of [beta]-adrenoceptor agonist on ciliary
motility, we measured ciliary beat frequency (CBF) of rabbit cultured
tracheal epithelial cells by photoelectric method and NO release by
specific amperometric sensors for this molecule in vitro. Salbutamol
increased CBF, an effect that was potentiated by superoxide
dismutase. Pretreatment of cells with NG-nitro-L-arginine methylester
(L-NAME) attenuated the salbutamol-induced increase in CBF, causing a
rightward displacement of the concentration-response curve by 2-2.5
log U, whereas D-NAME had no effect. The inhibitory effect of L-NAME
was reversed by L-arginine but not by D-arginine. Immersion of the
NO-selective electrode in the medium containing epithelial cells
detected baseline current of 4.6-14.5 pA, which was abolished by L
-NAME. Salbutamol dose dependently increased the concentration of NO
in the medium, the maximal increase being 56.2 +/- 5.3 nM (mean +/-
SEM, P < 0.001). These results suggest that NO is spontaneously
released by airway epithelium and that the enhanced release of this
molecule may play a role in the [beta]-adrenoceptor-mediated
stimulation of ciliary motility.
Received 21 October 1994; accepted in final form 13 December
1994.
APS Manuscript Number C629-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 7 March 1995.