Hiroshi Watanabe (1), Hiromichi Tsuru (2,*), Koji Yajin (1), Hiroko Kawamoto
(1) and Masashi Sasa (2)
(1) Department of Otorhinolaryngology and (2) Department of Pharmacology,
Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima
734-855I, Japan
(*) Present address for correspondence: Department of Pharmacology, Toho
University School of Medicine, 5-21-16 Ohmorinishi, Ohta-ku, Tokyo 143-8540,
Japan
Abstract: We have previously reported that there is non-adrenergic,
non-cholinergic (NANC) innervation in canine nasal mucosa and that the relaxation
response to electrical stimulation of the NANC nerve is mainly mediated
by nitric oxide (NO). In the present study, we examined the effect of cold
exposure (24C) on nitroxidergic nerve-mediated vasodilatation in isolated
canine nasal mucosa. Nasal mucosa strips, prepared from canine nasal septum
and moderately precontracted with methoxamine in the presence of atropine
and guanethidine, relaxed in response to transmural electrical stimulation
(square pulses of 0.5-msec duration, at 5 Hz and 25 V). The degree of relaxation
at 24C (55.4+/-13.2% of methoxamine-induced contraction, mean+/-S.D., n=6)
was significantly greater than that at 34C (33.8+/-8.6%, n=6). This phenomenon
was reversible. In contrast, the magnitude of relaxation responses to an
NO donor (sodium nitroprusside of 0.1 and 1 microM) remained unchanged by
cold exposure. These results suggest that the release of NO from the nitroxidergic
nerve endings is augmented by cold exposure and, thus, vasodilatation of
the nasal blood vessel is enhanced, thereby contributing to the swelling
of the nasal mucosa in cold conditions.
Keywords: Nasal mucosa (dog), Cold exposure, Nitric oxide, Nitroxidergic
nerve, Vasodilatation