The purpose of the present study was to characterize the cardiorespiratory effects of activation of 5-HT1A, 5-HT1B and 5-HT2 receptor subtypes at the intermediate area of the ventral surface of the medulla. The agonists (+/-)-8-hydroxy-2-(di-N-propylamino)
tetralin hydrobromide (8-OH-DPAT), 1-[3-(trifluoromethyl)phenyl]-
piperazine hydrochloride (
TFMPP) and (+/-)-1-(2,5-di-methoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) were used to activate these receptor subtypes, respectively. Application of each
drug to the intermediate area produced a different profile of cardiorespiratory effects.
8-OH-DPAT (0.0625-4.0 micrograms) produced dose-dependent
hypotension and
bradycardia, which were antagonized by the 5-HT1A antagonists
spiperone and
spiroxatrine. The
bradycardia was blocked by bilateral
vagotomy. No significant changes in respiratory motor outflow to the larynx or diaphragm were observed after application of
8-OH-DPAT.
TFMPP (10-1000 micrograms) also produced a dose-dependent
hypotension and
bradycardia. However, these effects were not antagonized by
spiperone or blocked by
vagotomy. A decrease in the amplitude of the recurrent laryngeal and phrenic nerve signals was observed after application of the highest dose of
TFMPP. In contrast to the effects of
8-OH-DPAT and
TFMPP, DOI (0.3-100 micrograms) produced an increase in blood pressure without any change in heart rate. Recurrent laryngeal and phrenic nerve activities were depressed, as was respiratory rate, after application of DOI. Both the cardiovascular and respiratory effects of DOI were blocked by the
5-HT2 antagonist ketanserin. These results indicate that activation of ventral medullary
5-HT receptor subtypes produces unique effects on cardiorespiratory activity.