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Angiotensin II inhibits inward rectifier K+ channels in rabbit coronary arterial smooth muscle cells through protein kinase Calpha

Cited 26 time in Web of Science Cited 31 time in Scopus
Authors
Park, Won Sun; Kim, Nari; Youm, Jae Boum; Warda, Mohamad; Ko, Jae-Hong; Kim, Sung Joon; Earm, Yung E.; Han, Jin
Issue Date
2006-01-31
Publisher
Elsevier
Citation
Biochem Biophys Res Commun. 2006 Mar 17;341(3):728-35. Epub 2006 Jan 19.
Keywords
Angiotensin II/*pharmacologyAnimalsCalcium/chemistry/metabolismCations, Divalent/chemistryCells, CulturedElectrophysiologyFemaleIsoenzymes/antagonists & inhibitors/classification/metabolismMaleMuscle, Smooth, Vascular/*drug effects/*metabolismMyocytes, Smooth Muscle/*drug effects/*metabolismPatch-Clamp TechniquesPotassium Channels, Inwardly Rectifying/*metabolismProtein Kinase C-alpha/antagonists & inhibitors/*metabolismProtein Kinase Inhibitors/pharmacologyRabbitsReceptor, Angiotensin, Type 1/metabolismType C Phospholipases/antagonists & inhibitors/metabolism
Abstract
We investigated the effects of the vasoconstrictor angiotensin (Ang) II on the whole cell inward rectifier K(+) (Kir) current enzymatically isolated from small-diameter (<100 microm) coronary arterial smooth muscle cells (CASMCs). Ang II inhibited the Kir current in a dose-dependent manner (half inhibition value: 154 nM). Pretreatment with phospholipase C inhibitor and protein kinase C (PKC) inhibitors prevented the Ang II-induced inhibition of the Kir current. The PKC activator reduced the Kir currents. The inhibitory effect of Ang II was reduced by intracellular and extracellular Ca(2+) free condition and by Go6976, which inhibits Ca(2+)-dependent PKC isoforms alpha and beta. However, the inhibitory effect of Ang II was unaffected by a peptide that selectively inhibits the translocation of the epsilon isoform of PKC. Western blot analysis confirmed that PKCalpha, and not PKCbeta, was expressed in small-diameter CASMCs. The Ang II type 1 (AT(1))-receptor antagonist CV-11974 prevented the Ang II-induced inhibition of the Kir current. From these results, we conclude that Ang II inhibits Kir channels through AT(1) receptors by the activation of PKCalpha.
ISSN
0006-291X (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16442501

https://hdl.handle.net/10371/24778
DOI
https://doi.org/10.1016/j.bbrc.2006.01.026
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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