2006年6月
The lipopolysaccharide-induced up-regulation of bradykinin B-2-receptor in the mouse heart is mediated by tumor necrosis factor-alpha and angiotensin
BIOLOGICAL & PHARMACEUTICAL BULLETIN
- ,
- ,
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- 巻
- 29
- 号
- 6
- 開始ページ
- 1143
- 終了ページ
- 1147
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1248/bpb.29.1143
- 出版者・発行元
- PHARMACEUTICAL SOC JAPAN
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 B2-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.
- リンク情報
- ID情報
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- DOI : 10.1248/bpb.29.1143
- ISSN : 0918-6158
- PubMed ID : 16755007
- Web of Science ID : WOS:000238470500012