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Circulation Research. 2000;87:272-274

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(Circulation Research. 2000;87:272.)
© 2000 American Heart Association, Inc.


Editorials

Cardiac Gap Junction Remodeling by Stretch

Is It a Good Thing?

Gregory E. Morley, José Jalife

From the Department of Pharmacology, SUNY Upstate Medical University, Syracuse, NY.

Correspondence to José Jalife, MD, Department of Pharmacology, SUNY Upstate Medical University, 766 Irving Ave, Syracuse, NY 13210. E-mail jalifej@upstate.edu


Key Words: mechanical forces • pulsatile stress • cell-to-cell communication • conduction velocity • optical mapping • immunohistochemistry


*    Introduction
 
Cardiac cells contract and are also normally exposed to the mechanical events in their surroundings. It is now well established that both cardiac gene expression and protein synthesis are subject to regulation by mechanical forces, including stretch. For example, mechanical stretch is known to be one of the most important stimuli leading to cardiac hypertrophy,1 2 3 4 5 and recent studies indicate that cardiac myocyte hypertrophy is stimulated in vitro by specific directions and degrees of stretch.6 Similarly, certain stretch-sensitive sarcolemmal ion channels and exchangers have been found in cardiac myocytes7 and have been implicated in the mechanism of stretch-induced arrhythmias.8 However, whereas signal transduction induced by mechanical stretch involves activation of a wide variety of second messenger systems,9 it remains to be determined which molecules are directly affected by stretch and which are the processes whereby mechanical stimuli trigger intracellular signaling pathways to activate protein kinase cascades and produce changes in function.

The process of filling and ejecting blood subjects the cells of the heart to repetitive pulsatile stress. Our understanding of the basic electrophysiology underlying the cardiac action potential and its propagation across cells is largely on the basis of patch clamp data and isolated tissue experiments in the absence of mechanical stress. On the other hand, whole-heart electrophysiological mapping studies are often carried out in in situ functioning hearts. In either case, the role of mechanical stress in impulse initiation and propagation has not been adequately addressed. In addition, although stretch is thought to play an important role in cardiac . . . [Full Text of this Article]




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