What are roles of bradykinin and prostaglandins in promoting pain and edema after tissue injury?

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Multiple Choice

What are roles of bradykinin and prostaglandins in promoting pain and edema after tissue injury?

Inflammatory mediators released after tissue injury set up both pain and swelling. Bradykinin directly activates nociceptors, producing pain, and it increases vascular permeability, allowing fluid to leak into the tissue and cause edema. Prostaglandins, especially PGE2, don’t trigger nociceptors as strongly on their own, but they make nociceptors more responsive by lowering their activation threshold and by amplifying the effect of bradykinin and other mediators. They also promote vasodilation, contributing to swelling. So the combination is that bradykinin directly drives pain and edema through nociceptor activation and increased permeability, while prostaglandins sensitize nociceptors and amplify pain.

Inflammatory mediators released after tissue injury set up both pain and swelling. Bradykinin directly activates nociceptors, producing pain, and it increases vascular permeability, allowing fluid to leak into the tissue and cause edema. Prostaglandins, especially PGE2, don’t trigger nociceptors as strongly on their own, but they make nociceptors more responsive by lowering their activation threshold and by amplifying the effect of bradykinin and other mediators. They also promote vasodilation, contributing to swelling. So the combination is that bradykinin directly drives pain and edema through nociceptor activation and increased permeability, while prostaglandins sensitize nociceptors and amplify pain.

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