期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2005
卷号：102
期号：12
页码：4643-4648
DOI：10.1073/pnas.0408844102
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Phosphatidylionsitol 4,5-bisphosphate (PIP2), a substrate of phospholipase C, has recently been recognized to regulate membrane-associated proteins and act as a signal molecule in phospholipase C-linked Gq-coupled receptor (GqPCR) pathways. However, it is not known whether PIP2 depletion induced by GqPCRs can act as receptor-specific signals in native cells. We investigated this issue in cardiomyocytes where PIP2-dependent ion channels, G protein-gated inwardly rectifying K+ (GIRK) and inwardly rectifying background K+ (IRK) channels, and various GqPCRs are present. The GIRK current was recorded by using the patch-clamp technique during the application of 10 {micro}M acetylcholine. The extent of receptor-mediated inhibition was estimated as the current decrease over 4 min while taking the GIRK current (IGIRK) value during a previous stimulation as the control. Each GqPCR agonist inhibited IGIRK with different potencies and kinetics. The extents of inhibition induced by phenylephrine, angiotensin II, endothelin-1, prostaglandin F2{alpha
关键词：phospholipase C ; cardiac myocyte ; phosphatidylinositol 4-kinase ; Gq-coupled receptor ; G protein-gated inwardly rectifying K+ channels
