POSSIBLE INVOLVEMENT OF THE EP, RECEPTOR SUBTYPE IN PGE(2)-INDUCED ENHANCEMENT OF THE HEAT RESPONSE OF NOCICEPTORS

Prostaglandin E, augments bradykimin- and heat-induced discharges of p olymodal receptors as studied in vitro preparations. Our previous stud y revealed the involvement of the EP, receptor subtype in the PGE, ind uced enhancement of the BK response [Brain Res. 632 (1993) 321-324]. T he agonist for EP, (butaprost; 10(-8) M) significantly augmented heat responses, but did not augment the BK responses at concentrations from 10(-8) to 10(-5) M; however, the agonist for EP, (MandB28767) or EP, (17-phenyl-trinor-PGE(2)) at 10-(7) M did not affect the heat response s. These findings indicate the involvement of the EP, receptor subtype in the augmenting effect of PGE, on heat responses.