The present study was designed to investigate the mechanism of gingival vasodilatation induced by electrical stimulation of the inferior alveolar nerve (IAN) in cats. A total of 55 young cats (2-4 kg) were anesthetized with pentobarbital sodium (30 mg/kg, i.v.). After IAN was surgically exposed, gingival blood flow (GBF) was continuously measured with the noninvasive technique of using a laser Doppler velocimeter (LDV). The systemic blood pressure was monitored during the experiment. Electrical stimulation of the distal end of the cut IAN led to a GBF increase with no alteration of the blood pressure in guanethidine treated cats. These increases were dependent on both the stimulus intensity (20-80 V) and the stimulus duration (0.2-5 sec). The GBF increases observed were reproducible for 100 min, when a resting period of 10 min was allowed between stimulations. The GBF increase by electrical stimulation of IAN was significantly inhibited by 66.8 +/- 7.3%, 51.1 +/- 3%, 37.8 +/- 4.6% (mean +/- S.E.M.) after i.v. injection of (D-Pro2, D-Try7,9)-substance P, triplennamine or methysergide, respectively. I.v. injection of atropine, propranolol, hexamethonium or cimetidine, on the other hand, had no effect on the GBF increase by electrical stimulation of IAN. These results suggest that gingival vasodilatation following electrical stimulation of IAN in cats is initiated by the peripheral release of substance P from sensory nerves, and that the substance P released, in turn, stimulates the mast cells to release histamine or serotonin which causes the vasodilatation.
|Number of pages||13|
|Journal||Shika Kiso Igakkai zasshi = Japanese journal of oral biology|
|Publication status||Published - 1989 Oct|
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