Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)
| Autor: | Etsuji Terazawa, Kimiaki Katanosaka, Fernando Queme, Toru Taguchi, Kenji Hirate, Yasuko Kozaki, Shiori Murase, Kazue Mizumura, Teru Matsuda, Hisako Urai, Hiroki Ota |
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| Rok vydání: | 2010 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Bradykinin Stimulation Rats Sprague-Dawley chemistry.chemical_compound Downregulation and upregulation Physical Conditioning Animal Internal medicine Delayed onset muscle soreness medicine Animals Muscle Skeletal Receptor Pain Measurement Nerve Fibers Unmyelinated business.industry General Neuroscience Antagonist Articles Electric Stimulation Rats Nerve growth factor Endocrinology chemistry Hyperalgesia Anesthesia medicine.symptom B2 Bradykinin Receptor business Mechanoreceptors Muscle Contraction |
| Zdroj: | The Journal of Neuroscience. 30:3752-3761 |
| ISSN: | 1529-2401 0270-6474 |
| Popis: | Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes delayed-onset muscle soreness (DOMS), a kind of muscular mechanical hyperalgesia. The substances that induce this phenomenon are largely unknown. Peculiarly, DOMS is not perceived during and shortly after exercise, but rather is first perceived after ∼1 d. Using B2bradykinin receptor antagonist HOE 140, we show here that bradykinin released during exercise plays a pivotal role in triggering the process that leads to muscular mechanical hyperalgesia. HOE 140 completely suppressed the development of muscular mechanical hyperalgesia when injected before LC, but when injected 2 d after LC failed to reverse mechanical hyperalgesia that had already developed. B1antagonist was ineffective, regardless of the timing of its injection. Upregulation of nerve growth factor (NGF) mRNA and protein occurred in exercised muscle over a comparable time course (12 h to 2 d after LC) for muscle mechanical hyperalgesia. Antibodies to NGF injected intramuscularly 2 d after exercise reversed muscle mechanical hyperalgesia. HOE 140 inhibited the upregulation of NGF. In contrast, shortening contraction or stretching induced neither mechanical hyperalgesia nor NGF upregulation. Bradykinin together with shortening contraction, but not bradykinin alone, reproduced lasting mechanical hyperalgesia. We also showed that rat NGF sensitized thin-fiber afferents to mechanical stimulation in the periphery after 10–20 min. Thus, NGF upregulation through activation of B2bradykinin receptors is essential (though not satisfactory) to mechanical hyperalgesia after exercise. The present observations explain why DOMS occurs with a delay, and why lengthening contraction but not shortening contraction induces DOMS. |
| Databáze: | OpenAIRE |
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