The attenuation mechanism of bradykinin B2 receptor desensitization through prostaglandin EP3 receptor

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Repeated administration of bradykinin (BK), which is one of the endogenous algesic substances, induces desensitization of B2 receptor. Activation of prostaglandin (PG) E2 EP3 receptor attenuates B2 receptor desensitization, leading to increased pain. Our findings indicate a possibility that prostaglandin enhances both internalization of B2R bound to BK and recycling of the internalized bradykinin B2R through EP3R, and this might be a mechanism for sensitizing the BK response of nociceptors by prostaglandin E2.