Table 19-1 Tissue chemicals affecting polymodal nociceptors
| Compound | Origin | Mechanism of action | Mode of action on nociceptive fiber |
|---|---|---|---|
| Protons (acid) | Tissue metabolism. | Increased ion conductance. | Activation. |
| Potassium | Injured cells. | Direct effect on membrane potential. | Activation. |
| Adenosine triphosphate | Tissue cells. | Increased ion conductance. | Activation. |
| Bradykinin | Tissue protease cleves kininogen. | Receptor acts through second messengers. | Activates through second messengers. |
| Histamine | Mast cells (release triggered by substance P). | Vasodilation and increased vascular permiability. | Activates pain fibers in high concentration; allows substances to enter tissues. |
| Eicosanoids (prostaglandin) | Many cells when injured (including nerve terminals). | Receptor inked to second messenger (cyclic AMP). | Mainly a sensitizer of nociceptors. |
| Leukotrines | From cells of immune system. | Trigger release of pain-producing compounds from other cells. | Acts indirectly. |
| Cytokines (e.g., interleukin, tumor necrosis factor, interferons, etc.) | From cells of immune system. | Probably act by causing synthesis of other compounds (such as prostaglandin). | Acts indirectly. |
| Substance P | From nociceptive afferent nerve fibers. | Works by causing release of histamine, serotonin and prostaglandin as well as release of leukotrines and cytokines. | Acts indirectly. |
| Catecholamines | Sympathetic nerve terminals. | Increases tissue prostaglandin synthesis and may directly activate injured axons. | Mostly acts indirectly. |
| Nerve growth factors | Produced in inflamed tissues. | Alters gene expression in sensory nerve fibers. | Acts indirectly. |
| Serotonin | Platelets and mast cells. | Receptor subtypes (both ion channel and second-messenger). | Sensitization more important than direct activation; increase calcium currents via second messengers. |
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