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(Circulation Research. 2000;87:427.)
© 2000 American Heart Association, Inc.

Editorials

A Case for Myoendothelial Gap Junctions

Donald G. Welsh, Mark T. Nelson

From the Department of Pharmacology, University of Vermont, Burlington, Vt.

Correspondence to Dr Mark Nelson, Room B-303, Given Building, Department of Pharmacology, University of Vermont, Burlington, VT 05404. E-mail nelson@salus.med.uvm.edu

Key Words: endothelium • smooth muscle • gap junctions

	Introduction

 
Tissue perfusion is controlled by a network of resistance arteries linked in series and parallel with one another. It has been long appreciated that blood flow resistance is distributed throughout this network, and thus substantive change in perfusion only occurs when coupled arteries respond in a coordinated fashion. To coordinate vasomotor responses, vascular cells must communicate with one another. This communication is, in part, facilitated by gap junctions, which are intercellular pores that permit charged ions, second messenger molecules, and small metabolites to pass among adjacent cells. Gap junctions are formed by two hemichannels, each containing 6 connexin proteins. At present, the connexin gene family is comprised of 14 members, with the most predominant subtypes being Cx40 and Cx43 in vascular smooth muscle¹ and Cx37, Cx40, and Cx43 in endothelial cells.²

For gap junctions to form an electrical or diffusional conduit, vascular cells must lie in close apposition to each other. With few structural elements limiting the contact of adjacent smooth muscle cells or adjacent endothelial cells, it has been widely accepted that these cells are homologously coupled. Indeed, studies using connexin antibodies to characterize gap junctional distribution have substantiated this view.^{1 3 4} In contrast, the internal elastic lamina, a connective tissue layer that separates smooth muscle from the endothelium, has been presumed to prevent the formation of heterologous (ie, myoendothelial) gap junctions. However, some studies have shown that the internal elastic lamina is not contiguous and that endothelial cells can indeed penetrate this barrier, emerging in close apposition to the . . . [Full Text of this Article]

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