© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
NO and cholinergic signalling in the heart: divergent routes to regulatory phosphorylation of the cardiac L-type Ca2+ channel
Department of Pharmacology and Toxicology, SFB-Biomembranes Research Center, Karl-Franzens-University, Universitätsplatz 2, A-8010, Graz, Austria
*Tel.: +43-316-380-5570; fax: +43-316-380-9890. Email address: klaus.groschner@uni-graz.at
Received 27 August 2003;
| The first 10% of the full text of this article appears below. |
 |
1. Introduction |
|---|
Voltage-gated cardiac L-type channels (CaV1.2a) are a pivotal signalling element involved in the control of myocardial function by the autonomic nervous system. Dual control of Ca2+ entry into cardiac myocytes by sympathetic and parasympathetic stimuli is likely to converge on reversible phosphorylation of CaV1.2a channels, a process that is governed by cyclic nucleotide-dependent protein kinases. The molecular basis of this regulation, and in particular the role cGMP-dependent phosphorylation in cholinergic suppression of Ca2+ entry, is still obscure. In this issue of Cardiovascular Research, Schröder et al. [1] report that transgenic over-expression of cGMP-dependent kinase I (PKG I) promotes the inhibitory modulation of cardiac Ca2+ channels by the
|
2. A transgenic animal model challenges the "yin-yang" hypothesis |
|---|
|
3. PKG-I may control Cav1.2 channels via multiple target sites |
|---|
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Yang, G. Liu, S. I. Zakharov, A. M. Bellinger, M. Mongillo, and S. O. Marx Protein Kinase G Phosphorylates Cav1.2 {alpha}1c and {beta}2 Subunits Circ. Res., August 31, 2007; 101(5): 465 - 474. [Abstract] [Full Text] [PDF]
|
|