Vagal visceral inputs to the nucleus of the solitary tract: involvement in a parasympathetic reflex vasodilator pathway in the rat masseter muscle.
The present study examined whether vagal visceral inputs are involved in parasympathetic reflex vasodilatation in the masseter muscle in urethane-anesthetized and cervically sympathectomized rats. Electrical stimulation of the central cut end of the cervical vagus nerve (VN) including visceral afferent fibers, which consisted of cervical/thoracic branches (heart and lungs) and abdominal branches (entire gastrointestinal tract), elicited intensity- and frequency-dependent increases of blood flow in the masseter muscle (MBF). Activation of the abdominal VN inferior to the diaphragm failed to affect the MBF. MBF increases evoked by cervical VN stimulation were reduced significantly by hexamethonium. Pretreatment with atropine reduced the MBF increase evoked by VN stimulation significantly, whereas pretreatment with either propranolol or phentolamine had no effect on the response. MBF increases occurred with electrical stimulation of nucleus of the solitary tract (NTS), and these increases were significantly reduced by the administration of hexamethonium and atropine. MBF increases also occurred after microinjection of glutamate into the NTS in a dose-dependent manner. Microinjection of muscimol into the NTS caused a significant attenuation of the VN stimulation-induced MBF increases. Our results suggest that vagal visceral inputs passing to the NTS are involved in the parasympathetic reflex vasodilatation in the rat masseter muscle. The MBF increase evoked by the vagal-parasympathetic reflex mechanism occurred via visceral afferents running in the cervical VN, but not in the abdominal VN, suggesting that the vagal visceral afferents derived from cardiovascular and/or respiratory systems may play an important role in the regulation of the MBF.
Ishii
Hisayoshi
H
Division of Physiology, Department of Oral Biology, School of Dentistry, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.
Niioka
Takeharu
T
Izumi
Hiroshi
H
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001703:Biophysics; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation / Q000379:methods; D018755:GABA Agonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects*; D018738:Hexamethonium / Q000494:pharmacology; D017078:Laser-Doppler Flowmetry / Q000379:methods; D008046:Lip / Q000098:blood supply / Q000294:innervation; D008297:Male; D008406:Masseter Muscle / Q000098:blood supply; D009118:Muscimol / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012018:Reflex / Q000502:physiology*; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D018755:GABA Agonists; D018733:Nicotinic Antagonists; D010276:Parasympatholytics; D014665:Vasodilator Agents; D009118:Muscimol; D018738:Hexamethonium; D018698:Glutamic Acid; D001285:Atropine; D011433:Propranolol; D010646:Phentolamine