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1. The role of central 5-HT(1A) receptors in the control of the bradycardia and changes in central respiratory drive, renal nerve activity and blood pressure evoked by stimulating cardiopulmonary afferents with phenylbiguanide, baroreceptors by electrical stimulation of the aortic nerve and chemoreceptors by injections of sodium cyanide (NaCN) in atenolol-pretreated anaesthetized rabbits were studied. 2. Buspirone (100 micro g kg(-1); i.c.) potentiated the bradycardia (increase in R-R interval) and the changes in blood pressure and renal nerve activity evoked by all three reflexes. These effects could be attenuated by pretreatment with the 5-HT(1A) receptor antagonist WAY-100635 (100 micro g kg(-1)); i.v.), which alone had no effect on these reflex-evoked changes. However, WAY-100635 (100 micro g kg(-1); i.c.) did attenuate these reflex-evoked responses produced by activation of cardiopulmonary and aortic baroreceptors but not that caused by stimulation of chemoreceptors. When given i.v., buspirone was less effective in modulating the responses evoked by these three reflexes. 3. The present data are consistent with the view that central 5-HT(1A) receptors play a role in the reflex activation of cardiac preganglionic vagal motoneurones. However, although antagonists of 5-HT(1A) receptors affected the responses evoked by cardiopulmonary and aortic nerve afferents, they were not effective on chemoreceptor reflex-evoked changes. This suggests that 5-HT(1A) receptors play a different role in chemoreceptor pathways compared to that for the other reflexes. This may relate to the fact that the chemoreceptor afferents travel in the IXth (glossopharyngeal) nerve whilst the other afferents travel in the Xth (vagus) nerve and thus may use different central circuitry and neurotransmitters.

1. The effects of central application of 5-HT1A and 5-HT1B/1D receptor ligands on the reflex bradycardia, apnoea, renal sympathoexcitation and pressor response evoked by stimulating upper airway receptors with smoke in atenolol-pretreated anaesthetized rabbits were studied. 2. Intracisternal administration of the 5-HT1A receptor antagonists WAY-100635 (100 microg kg(-1)) and (-)pindolol (100 microg kg(-1)) significantly reduced the smoke-induced bradycardia, attenuated the pressor response and in the case of (-)pindolol, sympathetic nerve activity. The same dose of WAY-100635 i.v. was without effect. 3. Buspirone (200 microg kg(-1), i.c.) potentiated the reflex bradycardia. This action was prevented if the animals were pretreated with WAY-100635 (100 Hg kg(-1), i.v.) 4. (+)8-OH-DPAT (25 microg kg(-1), i.c.) attenuated the evoked bradycardia, pressor response, apnoea and renal sympathoexcitation. The attenuation of the apnoea and renal sympathoexcitation, but not the bradycardia or pressor response was prevented in animals pretreated with WAY-100635 (100 microg kg(-1), i.v.). The attenuation of the reflex bradycardia and the reduction in the renal sympathoexcitation were reduced by pretreatment with the 5-HT1B/1D receptor antagonist GR127935 (100 microg kg(-1), i.v.). 5. In WAY-100635 (100 microg kg(-1), i.v.) pretreated animals, sumatriptan (a 5-HT1B/1D receptor agonist) reduced the reflex bradycardia and the pressor response. The 5-HT1B/1D receptor antagonist GR127935 (20 microg kg(-1), i.c. or 100 microg kg(-1), i.v.) had no effect on the reflex responses. 6. In conclusion, the present data are consistent with the hypothesis that activation of central 5-HT1A receptors potentiate whilst activation of 5-HT1B/1D receptors attenuate the reflex activation of cardiac preganglionic vagal motoneurones evoked by stimulation of upper airway receptors with smoke in rabbits.