The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B(2)-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-alpha and Angiotensin II.
Our present study aimed to characterize the effects of lipopolysaccharide (LPS) on the expression of the bradykinin B(2)-receptor in the mouse heart, which may have a role in cardiac depression during sepsis. We found that LPS induced the up-regulation of B(2)-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Like LPS, tumor necrosis factor-alpha (TNF-alpha) but not interleukin (IL)-1-beta, IL-6 or endothelin-1 stimulated B(2)-receptor expression in cultured myocytes. The effect of LPS on the expression of B(2)-receptor mRNA was also mimicked in cardiac myocytes by Ang II via Ang II type 1 (AT(1)-) receptor. Losartan, an AT(1)-receptor antagonist, inhibited about 50% of the LPS-induced up-regulation of B(2)-receptor mRNA in the heart in vivo and in cultured cardiac myocytes in vitro. Furthermore, the up-regulation of B(2)-receptor mRNA by either LPS or Ang II in cultured myocytes was abolished by anti-TNF-alpha antibody. These results suggest that the up-regulation of cardiac B(2)-receptor expression by LPS is mediated through TNF-alpha, which is produced in the myocardium by two different mechanisms in an AT(1)-receptor-dependent and independent manners, implying the role of the cardiac kallikrein-kinin system in the development of cardiac dysfunction during sepsis.[1]References
- The Lipopolysaccharide-Induced Up-Regulation of Bradykinin B(2)-Receptor in the Mouse Heart Is Mediated by Tumor Necrosis Factor-alpha and Angiotensin II. Yayama, K., Hiyoshi, H., Sugiyama, K., Okamoto, H. Biol. Pharm. Bull. (2006) [Pubmed]
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