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(Circulation Research. 2007;101:1219.)
© 2007 American Heart Association, Inc.

Editorials

Which Connexins Connect?

Tudor M. Griffith

From the Department of Diagnostic Radiology, Wales Heart Research Institute, School of Medicine, Cardiff University, UK.

Correspondence to Prof Tudor Griffith, Department of Diagnostic Radiology, Wales Heart Research Institute, School of Medicine, Cardiff University, Health Park, Cardiff, CF14 4XN UK. E-mail griffith@cardiff.ac.uk

See related article, pages 1292–1299

Key Words: gap junction • electrotonic • EDHF • endothelium • smooth muscle

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Electrical signaling via gap junctions modulates vascular function via 2 physiologically interrelated mechanisms, namely dilations/constrictions that propagate longitudinally along the vessel wall,^1–4 and the EDHF phenomenon, in which relaxation is facilitated by the transmission of endothelial hyperpolarization to smooth muscle via a radial myoendothelial pathway.⁵ Gap junctions are composed from 2 hemichannels, each constructed from 6 connexin (Cx) protein subunits, whose alignment across the extracellular space permits intercellular diffusion of ions and small molecules <1 kDa in size and confers electrical continuity. Coupling is enhanced by the clustering of up to several hundred individual gap junction channels to form plaques that can be visualized by immunostaining at points of cell–cell contact. Vascular cells variably express 4 connexin subtypes (Cxs 37, 40, 43, and 45) with protein expression generally being more abundant in the endothelium than in smooth muscle cells. Most commonly, endothelial plaques contain Cx37 and Cx40 and medial plaques contain Cx43. This distribution is seen, for example, in the rabbit iliac artery in which synthetic peptides selectively targeted against Cx37 and Cx40 attenuate endothelium-dependent subintimal smooth muscle hyperpolarization, whereas peptides targeted against Cx43 attenuate the spread of medial hyperpolarization.⁶ In muscular arteries electrical signaling pathways thus appear to correlate closely with immunostaining findings.

In this issue of Circulation Research Wolfle and colleagues¹ have analyzed longitudinal conduction in mice with replacement of Cx40 by "knock in" of Cx45 (denoted as Cx40KI45 mice). Responses were initiated by localized application of the endothelium-dependent dilators acetylcholine (ACh) and bradykinin (BK) to cremasteric arterioles . . . [Full Text of this Article]

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