Absence of diabetic hyperalgesia in bradykinin B-1 receptor-knockout mice

Absence of diabetic hyperalgesia in bradykinin B-1 receptor-knockout mice

Autor Gabra, B. H. Google Scholar
Merino, V. F. Google Scholar
Bader, M. Google Scholar
Pesquero, J. B. Google Scholar
Sirois, P. Google Scholar
Instituição Univ Sherbrooke
Max Delbruck Ctr Mol Med
Universidade Federal de São Paulo (UNIFESP)
Resumo Experimental evidence has shown that the inducible bradykinin (BK) B-1 receptor (BKB1-R) subtype is involved in the development of hyperalgesia associated with type 1 diabetes. Selective BKB1-R antagonists inhibited, whereas selective agonists increased the hyperalgesic activity in diabetic mice in thermal nociceptive tests. Here we evaluate the development of diabetic hyperalgesia in a BKB1-R-knockout (KO) genotype compared to wild-type (WT) mice, the BKB1-R-KO mice were backcrossed for 10 generations to C57BL/6 genetic background before use in the experiments. Diabetes was induced by streptozotocin (STZ) and thermal nociception was assessed by the hot plate and tail immersion tests. the hyperalgesia observed in wild type mice was totally absent in the BKB1-R-KO mice. Furthermore, the selective BKB1-R agonist, desArg(9)BK, significantly increased the hyperalgesic activity in diabetic WT mice but had no effect on nociceptive responses in diabetic BKB1-R-KO mice. Taken together, the results confirm the crucial role of the BKB1-R, upregulated alongside inflammatory diabetes, in the development of diabetes-induced hyperalgesia. (C) 2004 Elsevier B.V. All rights reserved.
Assunto type 1 diabetes
bradykinin B-1 receptor
Idioma Inglês
Data 2005-04-15
Publicado em Regulatory Peptides. Amsterdam: Elsevier B.V., v. 127, n. 1-3, p. 245-248, 2005.
ISSN 0167-0115 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 245-248
Fonte http://dx.doi.org/10.1016/j.regpep.2004.12.003
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000227023900031
URI http://repositorio.unifesp.br/handle/11600/28254

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