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