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Dołączył: 03 Mar 2011
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 Wysłany: Pon 16:10, 07 Mar 2011 Temat postu: tory burch reva dtd lug gmj onx |
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Captopril of bradykinin on neonatal rat cardiac fibroblasts inhibit the proliferation of cells
Part of the role can be antagonistic AnglI:. Recent studies have reported that ACEI is B receptor agonists, can promote JCiinCardioI (China),[link widoczny dla zalogowanych], Sep2005. Vol21, No9B receptor expression: thus, receptors may be partially mediated the role of ACEI. Ang Ⅱ receptor in turn activated by AT BK / NO pathway,[link widoczny dla zalogowanych], inhibit the development of myocardial fibrosis:, suggesting that NO may be anti-cardiac hypertrophy and myocardial fibrosis plays an important role. NO signal transduction pathway through to generate a negative growth factor in the role of cGMP,[link widoczny dla zalogowanych], which the proliferation of many cells with negative regulatory role. In addition, cGMP may be the BK / NO inhibited the proliferation of CFs part of a cell regulator. CFs in the regulation of proliferation and play an important role:. This study demonstrates that blocking BK by HOE 140, the role of a, the cell culture supernatants and intracellular cGMP No content was significantly lower, indicating that BK-mediated proliferative effect of captopril against CFs generated with NO and cGMP on , which Kim et al: Study conclusions are consistent. In summary, captopril can inhibit the proliferation of CFs,[link widoczny dla zalogowanych], the development of cardiac hypertrophy have some reverse effect,[link widoczny dla zalogowanych], which might in part by the BK receptor-mediated by the J3, and with the BK / NO / cGMP signaling transduction pathways involved in regulation. However, the specific regulatory mechanisms remains to be further studied.
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