著者

石井 久淑 新岡 丈治 和泉 博之

出版者

日本生理学会

雑誌

日本生理学会大会発表要旨集

巻号頁・発行日

vol.2006, pp.202-202, 2006

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The sympathetic nerve (SN) has been reported to be involved in the development of jaw muscle dysfunctions because the masseter muscle pain is usually accompanied with the increase in the SN activity. We have recently reported that there are parasympathetic (PS) vasodilator fibers in the rat masseter muscle and that these fibers would be involved in the regulation of the hemodynamics of jaw muscles (J. Physiol. 569, 617-629, 2005). It is still unclear whether there is an interaction between the PS vasodilatation (PSV) in the masseter muscle and the SN activity. The present study was thus designed to examine 1) the effect of SN activation on the PSV in the masseter muscle, and 2) the neural mechanisms mediating the effect in anesthetized rats. The PS mediated masseter muscle blood flow (MBF) increases were evoked by electrical stimulation of the central cut end of the lingual nerve. The magnitudes of MBF increase were significantly reduced by ongoing electrical stimulation of the superior cervical sympathetic trunk in a frequency-dependent manner (0.5-10 Hz). Pretreatment with BIBP 3226, a neuropeptide Y (NPY) Y1 receptor antagonist, significantly reduced 30-40% in this inhibition, but phentolamine had no effect. The present study indicates that the excessive SN activation inhibits the PSV in the masseter muscle, suggesting a potential role in the etiology of jaw muscle dysfunctions. This inhibitory action may be due to an interaction of the PS vsodilator fibers and NPY that would be released from sympathetic fibers. <b>[J Physiol Sci. 2006;56 Suppl:S202]</b>