Central 5‐HT 7 receptors are critical for reflex activation of cardiac vagal drive in anaesthetized rats

5‐Hydroxytryptamine (5‐HT; serotonin)‐containing neurones contribute to reflex activation of parasympathetic outflow in a number of species, but the 5‐HT receptors mediating these effects have yet to be fully determined. The present experiments demonstrate that central 5‐HT 7 receptors are involved in the vagal bradycardia evoked during the cardiopulmonary reflex, baroreflexes and the chemoreflex, as well as other autonomic changes caused by these reflexes. The experiments examined the effects of the selective 5‐HT 7 receptor antagonists SB‐269970 and SB‐656104 on these reflexes. For the cardiopulmonary reflex, when compared to time‐matched vehicle control experiments, intracisternal application of SB‐269970 (30–300 μg kg −1 , i.c. ) dose‐dependently attenuated the evoked bradycardia. At the highest dose, SB‐269970 also attenuated the reflex hypotension and sympathoinhibition. The structurally different 5‐HT 7 receptor antagonist SB‐656104 (100 μg kg −1 , i.c. ) similarly attenuated the reflex bradycardia and hypotension. SB‐269970 (100 μg kg −1 , i.c. ) also attenuated the bradycardias evoked by electrical stimulation of aortic nerve afferents and the baroreflex evoked by the pressor response to phenylephrine (3–25 μg kg −1 , i.v. ). The gain of the baroreflex was also significantly attenuated (0.15 ± 0.06 versus 0.34 ± 0.06 ms mmHg −1 ). Finally, SB‐269970 (100 μg kg −1 , i.c. ) significantly attenuated both the bradycardia and sympathoexcitation evoked by the chemoreflex. These data indicate that central 5‐HT 7 receptors play an important facilitatory role in the reflex activation of vagal outflow to the heart.