The release of PGs from the isolated perfused rabbit ear was measured by means of a radioimmunoassay.
Bradykinin in dose dependent amounts released mainly PGE (presumably PGE1) and in much smaller amounts also PGF.
Bradykinin released similar amounts of PGE in innervated and chronically denervated ears.
Indomethacin completely prevented the PGE release by bradykinin.
ACh showed a much lower efficacy than bradykinin in releasing PGE and PGF. Synthetic substance P was devoid of any PGE releasing action.
It is concluded that bradykinin increases its own algesic action by a concomitant rapid stimulation of the PGE synthesis, thus providing a mechanism for the facilitation of its own algesic action.
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Lembeck, F., Popper, H. & Juan, H. Release of prostaglandins by bradykinin as an intrinsic mechanism of its algesic effect. Naunyn-Schmiedeberg's Arch. Pharmacol. 294, 69–73 (1976). https://doi.org/10.1007/BF00692786
- Afferent nerve endings
- Prostaglandin release