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In this study, we used the BK receptor B1\/B2 double\u2010knockout (B1B<jats:sub>2<\/jats:sub><jats:sup>\u2010\/\u2010<\/jats:sup>) mice to observe the role of BK receptor in cardiotoxicity induced by DOX and the underlying mechanisms. DOX induced myocardial injury with increased serum levels of AST, CK, and LDH, upregulated tissue expression of bradykinin B1\/B2 receptor, FABP4 and iNOS, and downregulated expression of eNOS. However, these altered releases of myocardial enzyme and the expression level of iNOS were significantly prevented in the B1B2<jats:sup>\u2010\/\u2010<\/jats:sup> mice. We concluded that the activation of both B1 and B2 receptors of BK were involved in the DOX\u2010induced acute myocardial injury, possibly mediated through iNOS signaling pathways.<\/jats:p>","DOI":"10.1002\/jbt.23393","type":"journal-article","created":{"date-parts":[[2023,7,6]],"date-time":"2023-07-06T11:14:25Z","timestamp":1688642065000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Bradykinin receptor participates in doxorubicin\u2010induced cardiotoxicity by modulating iNOS signal pathway"],"prefix":"10.1002","volume":"37","author":[{"given":"Xueyan","family":"Chen","sequence":"first","affiliation":[{"name":"The Key Laboratory of Neural and Vascular Biology, Ministry of Education Hebei Medical University Shijiazhuang P. R. China"},{"name":"Department of Pharmacology, The Key Laboratory of Pharmacology and Toxicology for New Drugs Hebei Medical University  Shijiazhuang P. R. 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