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- Kazue Mizumura, Takeshi Sugiura, Kimiaki Katanosaka, Ratan K Banik, and Yasuko Kozaki.
- Division of Stress Recognition and Response, Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan. mizu@riem.nagoya-u.ac.jp
- Exp Brain Res. 2009 Jun 1;196(1):53-65.
AbstractBradykinin is an endogenous nonapeptide known to induce pain and hyperalgesia to heat and mechanical stimulation. Correspondingly, it excites nociceptors in various tissues and sensitizes them to heat, whereas sensitizing effect on the mechanical response of nociceptors is not well established. Protein kinase C and TRPV1 contribute to the sensitizing mechanism of bradykinin to heat. In addition, TRPA1 and other ion channels appear to contribute to excitation caused by bradykinin. Finally, prostaglandins sensitize bradykinin-induced excitation in normal tissues by restoring desensitized responses due to the inhibition of protein kinase A.
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