Kubo Y, Reuveny E, Slesinger P A, Jan Y N, Jan L Y
Howard Hughes Medical Institute, University of California, San Francisco 94143-0724.
Nature. 1993 Aug 26;364(6440):802-6. doi: 10.1038/364802a0.
Parasympathetic nerve stimulation causes slowing of the heart rate by activation of muscarinic receptors and the subsequent opening of muscarinic K+ channels in the sinoatrial node and atrium. This inwardly rectifying K+ channel is coupled directly with G protein. Based on sequence homology with cloned inwardly rectifying K+ channels, ROMK1 (ref. 11) and IRK1 (ref. 12), we have isolated a complementary DNA for a G-protein-coupled inwardly rectifying K+ channel (GIRK1) from rat heart. The GIRK1 channel probably corresponds to the muscarinic K+ channel because (1) its functional properties resemble those of the atrial muscarinic K+ channel and (2) its messenger RNA is much more abundant in the atrium than in the ventricle. In addition, GIRK1 mRNA is expressed not only in the heart but also in the brain.
副交感神经刺激通过激活毒蕈碱受体以及随后在窦房结和心房中打开毒蕈碱钾通道，导致心率减慢。这种内向整流钾通道直接与G蛋白偶联。基于与克隆的内向整流钾通道ROMK1（参考文献11）和IRK1（参考文献12）的序列同源性，我们从大鼠心脏中分离出一种G蛋白偶联内向整流钾通道（GIRK1）的互补DNA。GIRK1通道可能对应于毒蕈碱钾通道，因为（1）其功能特性类似于心房毒蕈碱钾通道，（2）其信使RNA在心房中的丰度远高于心室。此外，GIRK1 mRNA不仅在心脏中表达，也在大脑中表达。
