Possible involvement of the EP2 receptor subtype in PGE2-induced enhancement of the heat response of nociceptors.
Prostaglandin E2 augments bradykinin- and heat-induced discharges of polymodal receptors as studied in vitro preparations. Our previous study revealed the involvement of the EP3 receptor subtype in the PGE2 induced enhancement of the BK response [Brain Res. 632 (1993) 321-324]. The agonist for EP2 (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 EP3 (M&B28767) or EP1 (17-phenyl-trinor-PGE2) at 10(-7) M did not affect the heat responses. These findings indicate the involvement of the EP2 receptor subtype in the augmenting effect of PGE2 on heat responses.
Department of Neural Regulation, Nagoya University, Japan.
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Kumazawa
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Mizumura
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Koda
D000527:Alprostadil / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D004285:Dogs; D006358:Hot Temperature; D066298:In Vitro Techniques; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology*; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology; D018078:Receptors, Prostaglandin E / Q000819:agonists / Q000502:physiology*; D013737:Testis / Q000294:innervation*; D013997:Time Factors
D011458:Prostaglandins E; D011459:Prostaglandins E, Synthetic; D018078:Receptors, Prostaglandin E; D000527:Alprostadil; C048491:butaprost; D001920:Bradykinin