Mueller Sylvia, Paegelow Inge, Reissmann Siegmund
Institute of Biochemistry and Biophysics, Biological and Pharmaceutical Faculty, Friedrich-Schiller-University Jena, Jena, Germany.
Department of Experimental and Clinical Pharmacology and Toxicology, University of Rostock, Rostock, Germany.
Signal Transduct. 2006 Feb;6(1):5-18. doi: 10.1002/sita.200500061. Epub 2006 Jan 17.
Potentiation of hormone actions can occur by different mechanisms, including inhibition of degrading enzymes, interaction with the hormone receptor leading to stabilization of bioactive conformation or leading to receptor homo- and hetero-oligomerization, receptor phosphorylation and dephosphorylation or can occur by directly influencing the signal transduction and ion channels. In this review the potentiation of bradykinin actions in different systems by certain compounds will be reviewed. Despite many long years of experimental research and investigation the mechanisms of potentiating action remain not fully understood. One of the most contradictory findings are the distinct differences between the inhibition of the angiotensin I-converting enzyme and the potentiation of the bradykinin induced smooth muscle reaction. Contradictory findings and hypothesized mechanisms in the literature are discussed in this review and in some cases compared to own results. Investigation of potentiating actions was extended from hypotension, smooth muscle reaction and cellular actions to activation of immunocompetent cells. In our opinion the potentiation of bradykinin action can occur by different mechanisms, depending on the system and the applied potentiating factor used.
激素作用的增强可通过不同机制发生，包括抑制降解酶、与激素受体相互作用导致生物活性构象稳定或导致受体同源和异源寡聚化、受体磷酸化和去磷酸化，或者可通过直接影响信号转导和离子通道而发生。在本综述中，将对某些化合物在不同系统中增强缓激肽作用的情况进行综述。尽管经过多年的实验研究和调查，但增强作用的机制仍未完全明了。最矛盾的发现之一是血管紧张素I转换酶抑制与缓激肽诱导的平滑肌反应增强之间存在明显差异。本综述将讨论文献中的矛盾发现和假设机制，并在某些情况下与我们自己的结果进行比较。对增强作用的研究已从低血压、平滑肌反应和细胞作用扩展到免疫活性细胞的激活。我们认为，缓激肽作用的增强可通过不同机制发生，这取决于所涉及的系统和所使用的增强因子。
