Modulation of reflexly evoked vagal bradycardias by central 5-HT1A receptors in anaesthetized rabbits.
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.
Skinner
Matthew R
MR
Department of Physiology, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, U.K.
Ramage
Andrew G
AG
Jordan
David
D
D000758:Anesthesia; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001645:Biguanides / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001919:Bradycardia / Q000503:physiopathology*; D002065:Buspirone / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation; D008297:Male; D010879:Piperazines / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology; D011725:Pyridines / Q000494:pharmacology; D011817:Rabbits; D011985:Receptors, Serotonin / Q000187:drug effects / Q000502:physiology*; D044263:Receptors, Serotonin, 5-HT1; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D012702:Serotonin Antagonists / Q000494:pharmacology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D012966:Sodium Cyanide / Q000494:pharmacology; D014630:Vagus Nerve / Q000502:physiology*
D001645:Biguanides; D010879:Piperazines; D011725:Pyridines; D011985:Receptors, Serotonin; D044263:Receptors, Serotonin, 5-HT1; D012702:Serotonin Antagonists; D017366:Serotonin Receptor Agonists; D001262:Atenolol; C090413:N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide; D012966:Sodium Cyanide; D002065:Buspirone; C008846:phenyl biguanide