Ueda H, Yoshihara Y, Takagi H
Biochem Biophys Res Commun. 1986 Jun 13;137(2):897-902. doi: 10.1016/0006-291x(86)91164-2.
Kyotorphin (Tyr-Arg) at 1 to 100 microM increased the intracellular [Ca2+]i, determined with Quin-II in the slice and the entry of 45Ca2+ entry into synaptosomes of the lower brain stem of the rat. These effects were not antagonized by nifedipine nor verapamil. However, since this dipeptide caused no changes on the membrane potentials of the synaptosomes, measured with Rhodamine 6G, it is suggested that the kyotorphin-induced increase in the [Ca2+]i may be due not to effects on the voltage dependent Ca2+ channels and Na+-Ca2+ exchange mechanisms caused by the changes of the membrane potentials, but to the specific receptor (kyotorphin receptor)-mediated mechanisms.
京都啡肽（酪氨酰-精氨酸）在1至100微摩尔浓度下可增加细胞内钙离子浓度（[Ca2+]i），这是通过在脑切片中使用喹啉-Ⅱ以及45Ca2+进入大鼠脑干下部突触体来测定的。这些作用不受硝苯地平或维拉帕米的拮抗。然而，由于这种二肽对用罗丹明6G测量的突触体膜电位没有影响，因此提示京都啡肽诱导的[Ca2+]i增加可能不是由于膜电位变化对电压依赖性Ca2+通道和Na+-Ca2+交换机制的影响，而是由于特定受体（京都啡肽受体）介导的机制。
