Metabotropic Regulation of RhoA/Rho-Associated Kinase by L-type Ca Channels New Mechanism for Depolarization-Evoked Mammalian Arterial Contraction
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چکیده
Miguel Fernández-Tenorio, Cristina Porras-González, Antonio Castellano, Alberto del Mechanism for Depolarization-Evoked Mammalian Arterial Contraction Channels : New 2+ Metabotropic Regulation of RhoA/Rho-Associated Kinase by L-type Ca Print ISSN: 0009-7330. Online ISSN: 1524-4571 Copyright © 2011 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation Research doi: 10.1161/CIRCRESAHA.111.240127 2011;108:1348-1357; originally published online April 14, 2011; Circ Res. http://circres.ahajournals.org/content/108/11/1348 World Wide Web at: The online version of this article, along with updated information and services, is located on the http://circres.ahajournals.org/content/suppl/2011/04/14/CIRCRESAHA.111.240127.DC1.html Data Supplement (unedited) at:
منابع مشابه
Metabotropic regulation of RhoA/Rho-associated kinase by L-type Ca2+ channels: new mechanism for depolarization-evoked mammalian arterial contraction.
BACKGROUND Sustained vascular smooth muscle contraction is mediated by extracellular Ca(2+) influx through L-type voltage-gated Ca(2+) channels (VGCC) and RhoA/Rho-associated kinase (ROCK)-dependent Ca(2+) sensitization of the contractile machinery. VGCC activation can also trigger an ion-independent metabotropic pathway that involves G-protein/phospholipase C activation, inositol 1,4,5-trispho...
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Vascular smooth muscle cell (SMC) contraction is mediated in part by calcium influx through L-type voltage-gated Ca channels (VGCC) and activation of the RhoA/Rho kinase (ROK) signaling cascade. We tested the hypothesis that Ca influx through VGCCs regulates SMC differentiation marker expression and that these effects are dependent on RhoA/ROK signaling. Depolarization-induced activation of VGC...
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Rho-associated kinase (ROK) activation plays an important role in K+-induced contraction of rat caudal arterial smooth muscle (Mita et al., Biochem J. 2002; 364: 431–40). The present study investigated a potential role for tyrosine kinase activity in K+-induced RhoA activation and contraction. The non-selective tyrosine kinase inhibitor genistein, but not the src family tyrosine kinase inhibito...
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Membrane depolarization is critical to pulmonary arterial (PA) contraction. Both L-type Ca(2+) channels (Ca(L)) and Rho-kinase are important signaling components of this process and mitochondrial and non-mitochondrial generated superoxides can be part of the signaling process. Maturation and long-term hypoxia (LTH) each can modify depolarization-dependent contraction and the role of superoxides...
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RATIONALE In arterial myocytes, membrane depolarization-induced Ca(2+) release (DICR) from the sarcoplasmic reticulum (SR) occurs through a metabotropic pathway that leads to inositol trisphosphate synthesis independently of extracellular Ca(2+) influx. Despite the fundamental functional relevance of DICR, its molecular bases are not well known. OBJECTIVE Biophysical and pharmacological data ...
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