Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 2007;100:931-933
doi: 10.1161/01.RES.0000265133.89488.9b
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by de Wit, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by de Wit, C.
Related Collections
Right arrowRelated Article
(Circulation Research. 2007;100:931.)
© 2007 American Heart Association, Inc.


Editorials

Closing the Gap at Hot Spots

Cor de Wit

From the Institut für Physiologie, Universität Lübeck, Germany.

Correspondence to Dr Cor de Wit, Institut für Physiologie, Universität Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail dewit@uni-luebeck.de



See related article, pages 1026–1035


Key Words: connexin • Ca2+ microdomains • Na+/K+-pump • Na+-Ca2+-exchange


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

Coordination of cellular behavior is indispensable for vascular function. Because of the structural design of the vascular tree only an orchestrated diameter change along the vessel length increases conductance significantly and ensures optimal tissue perfusion. Mechanisms that suffice these needs include locally generated signals at upstream sites which reflect downstream requirements (flow-induced dilation)1 and longitudinal signal transmission through communication channels residing in the vessel wall itself which enable the synchronisation of cellular behavior. This latter is achieved by homocellular gap junctions which are composed of connexins that connect adjacent cells by intercellular low-resistance channels establishing a functional syncitium.2 Electrical communication through these channels is experimentally studied by locally initiated vasomotor responses which conduct along the vessel wall and promote synchronized dilations or constrictions of arteriolar segments reflecting the coordination of cellular behavior.3 Longitudinal communication through gap junctions is also required for the synchronisation of intracellular Ca2+ ([Ca2+]i) changes in smooth muscle and subsequent vasomotion, ie, rhythmic oscillations of vascular diameter. Although the physiological significance of vasomotion is still to be clearly defined it depends critically on Ca2+ release from intracellular stores which occurs in an oscillating fashion and the synchronization of [Ca2+]i transients through gap junctional communication.4,5 In addition, endothelial and smooth muscle cells are coupled heterocellularly (myoendothelial junctions) allowing the direct spread of current from the endothelium to the smooth muscle6 or other signaling molecules.7

The importance of gap junctional communication in vascular function contrasts with the poor knowledge of its regulation in vessels which is . . . [Full Text of this Article]


Related Article:

Interaction Between Na+/K+-Pump and Na+/Ca2+-Exchanger Modulates Intercellular Communication
Vladimir V. Matchkov, Helena Gustafsson, Awahan Rahman, Donna M. Briggs Boedtkjer, Sarah Gorintin, Anne Kirstine Hansen, Elena V. Bouzinova, Helle A. Praetorius, Christian Aalkjaer, and Holger Nilsson
Circ. Res. 2007 100: 1026-1035. [Abstract] [Full Text] [PDF]