Electrical communication in branching arterial networks

• Published in: American journal of physiology. Heart and circulatory physiology 2012-09, Vol.303 (6), p.H680-H692
• Main Authors: Tran, Cam Ha T, Vigmond, Edward J, Goldman, Daniel, Plane, France, Welsh, Donald G
• Format: Article
• Language: English
• Subjects: Animals; Blood vessels; Cell Communication; Cells; Computer Simulation; Cricetinae; Electric Conductivity; Electric Stimulation; Endothelial Cells - physiology; Gap Junctions - physiology; Hemodynamics; Homeostasis; Male; Membrane Potentials; Mesenteric Arteries - anatomy & histology; Mesenteric Arteries - physiology; Mesocricetus; Models, Cardiovascular; Myocytes, Smooth Muscle - physiology; Myography; Regional Blood Flow; Rodents; Sepsis; Simulation; Splanchnic Circulation; Vascular Biology and Microcirculation; Vascular Diseases - pathology; Vascular Diseases - physiopathology; Vasodilation; Veins & arteries
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00261.2012

Electrical communication and its role in blood flow regulation are built on an examination of charge movement in single, isolated vessels. How this process behaves in broader arterial networks remains unclear. This study examined the nature of electrical communication in arterial structures where vessel length and branching were varied. Analysis began with the deployment of an existing computational model expanded to form a variable range of vessel structures. Initial simulations revealed that focal endothelial stimulation generated electrical responses that conducted robustly along short unbranched vessels and to a lesser degree lengthened arteries or branching structures retaining a single branch point. These predictions matched functional observations from hamster mesenteric arteries and support the idea that an increased number of vascular cells attenuate conduction by augmenting electrical load. Expanding the virtual network to 31 branches revealed that electrical responses increasingly ascended from fifth- to first-order arteries when the number of stimulated distal vessels rose. This property enabled the vascular network to grade vasodilation and network perfusion as revealed through blood flow modeling. An elevation in endothelial-endothelial coupling resistance, akin to those in sepsis models, compromised this ascension of vasomotor/perfusion responses. A comparable change was not observed when the endothelium was focally disrupted to mimic disease states including atherosclerosis. In closing, this study highlights that vessel length and branching play a role in setting the conduction of electrical phenomenon along resistance arteries and within networks. It also emphasizes that modest changes in endothelial function can, under certain scenarios, impinge on network responsiveness and blood flow control.