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(Circulation Research. 2000;86:249.)
© 2000 American Heart Association, Inc.

Editorials

Myoendothelial Gap Junctions

The Gap Is There, but Does EDHF Go Through It?

Ingrid Fleming

From the Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.G-Universität, Frankfurt am Main, Germany.

Correspondence to Ingrid Fleming, Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.G-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany.

Key Words: endothelium • gap junctions • smooth muscle

	Introduction

 
The endothelium-derived autacoids, nitric oxide (NO) and prostacyclin (PGI₂), play a crucial role in the regulation of local vascular tone. However, these two factors alone cannot account for all of the endothelium-dependent dilator responses observed in a number of arteries, most notably in coronary, mesenteric, carotid, and renal arteries. Because endothelium-dependent, but NO synthase and cyclo-oxygenase inhibitor-insensitive dilator responses are associated with vascular smooth muscle hyperpolarization, the existence of a third dilator autacoid, an endothelium-derived hyperpolarizing factor (EDHF), has been proposed.

By monitoring the membrane potential of detector vascular smooth muscle cells situated downstream from donor endothelial cells, it is possible to monitor the production of an EDHF.¹ On the other hand, there has been no convincing demonstration of the transfer of an NO/PGI₂-independent hyperpolarizing and relaxing factor from one artery to another in classical bioassay experiments. For such a bioassay system to detect EDHF, the hyperpolarizing factor, like NO or PGI₂, must be able to permeate the endothelial cell membrane and diffuse down its concentration gradient to stimulate a target (in this case Ca²⁺-dependent K⁺ channels) on smooth muscle cells. There is however no reason to assume that the transfer of an EDHF from endothelial to smooth muscle cells in vivo involves the generation of a membrane-permeable hyperpolarizing compound, as the transfer of EDHF may take place via a direct intercellular pathway.

Not all arteries generate an EDHF or exhibit an NO/PGI₂-independent relaxation upon agonist stimulation, and the general rule of thumb is that . . . [Full Text of this Article]

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