Abstract
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-HT 1A receptor ligands 8-OH-DPAT (50 μg·kg −1) and buspirone (200 μg·kg −1). 8-OH-DPAT attenuated while buspirone potentiated the bradycardia. These results support the view that 5-HT 1A receptors play an important role in modulating the excitability of cardiac vagal motoneurones.
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