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Cardiovascular Research 2000 48(3):362-364; doi:10.1016/S0008-6363(00)00225-X
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Muscarinic regulation of cardiac L-type Ca2+ current

Fuhua Chen*

Pediatric Cardiology, University of California at Los Angeles, School of Medicine, 675 C.E. Young Drive South, MRL Rm. 3754, Los Angeles, CA 90095, USA

* Tel.: +1-310-825-7105; fax: +1-310-825-7458 fchen@mednet.ucla.edu

Received 4 September 2000; accepted 7 September 2000

The first 10% of the full text of this article appears below.

See article by Klein et al. [1] (pages 367–374) in this issue.


   1 Introduction
 
As discussed by Klein and his colleagues in this issue of Cardiovascular Research [1], cGMP is an important intracellular second messenger of various extracellular stimuli regulating L-type Ca2+ current (ICa-L) in both normal and failing hearts. It has been postulated that muscarinic agonists such as carbachol (CCh) bind to muscarinic receptors to promote formation of an activated inhibitory G protein–guanosine triphosphate (Gi-GTP) complex. Upon GTP binding, the heterotrimeric G protein dissociates into two moieties, Gi{alpha}-GTP and Giβ{gamma}. Gi{alpha} inhibits adenylyl cyclase (AC) [2,3] and decreases cyclic AMP (cAMP) concentration and thereby inhibits cAMP-dependent protein kinase (PKA). The final result is the inhibition of the phosphorylation of effectors such as . . . [Full Text of this Article]


   2 Role of cGMP and cGMP-dependent protein kinase
 

   3 Role of nitric oxide synthase
 

   4 Conclusion
 

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