Evidence for the ability of central 5-HT1A receptors to modulate the vagal bradycardia induced by stimulating the upper airways of anesthetized rabbits with smoke.

Cigarette smoke passed through the nasal cavity of atenolol pre-treated anesthetized spontaneously breathing rabbits caused a bradycardia which was significantly modified by intracisternal application of the 5-HT1A receptor ligands 8-OH-DPAT (50 micrograms.kg-1) and buspirone (200 micrograms.kg-1). 8-OH-DPAT attenuated while buspirone potentiated the bradycardia. These results support the view that 5-HT1A receptors play an important role in modulating the excitability of cardiac vagal motoneurones.