Kudo T, Kuroi M, Inoki R
Neuropeptides. 1986 May-Jun;7(4):391-7. doi: 10.1016/0143-4179(86)90032-6.
A possible relationship between met-enkephalin (ME)-like peptides and bradykinin (BK) in the rat incisor pulp was examined in in vitro experiments using whole pulp. ME-like peptide content in the pulp was increased by BK at a concentration of 1 microM, but not in higher concentrations, while the release of ME-like peptides from the pulp into the incubation medium was increased dose-dependently by BK. These effects of BK were inhibited by Des-Arg9-[Leu8]-BK, a potent BK-antagonist, suggesting that the effects of BK were mediated through a specific BK-receptor in the pulp. On the other hand, high K+ did not induce any increased release of ME-like peptides from the pulp and the BK effects were influenced neither in Ca++-free medium nor in the presence of ouabain. These results suggested that ME-like peptide releasing effect of BK was not due to depolarization of the cell membrane and was not active. In addition, kyotorphin, and enkephalin-releaser, could not only elicit a release of ME-like peptides from the pulp, but also a marked increase of the peptide content in the pulp. However, a combination of BK and kyotorphin attenuated the effect of BK or kyotorphin each other. These results suggested that there might be two kinds of mechanisms of ME-like peptide production in the pulp and those mechanisms might interfere mutually.
采用全牙髓体外实验研究了大鼠切牙髓中蛋氨酸脑啡肽(ME)样肽与缓激肽(BK)之间可能的关系。1 microM浓度的BK可使牙髓中ME样肽含量增加,但更高浓度时则无此作用,而BK可使牙髓中ME样肽向孵育培养基中的释放呈剂量依赖性增加。BK的这些作用被强效BK拮抗剂去精氨酸9-[亮氨酸8]-BK抑制,提示BK的作用是通过牙髓中特定的BK受体介导的。另一方面,高钾并未诱导牙髓中ME样肽释放增加,且在无钙培养基或哇巴因存在的情况下,BK的作用均未受影响。这些结果表明,BK的ME样肽释放作用并非由于细胞膜去极化,且不具有活性。此外,脑啡肽释放肽酪氨啡肽不仅可引起牙髓中ME样肽的释放,还可使牙髓中肽含量显著增加。然而,BK与酪氨啡肽联合使用会相互减弱彼此的作用。这些结果提示,牙髓中可能存在两种ME样肽产生机制,且这些机制可能相互干扰。