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Electrical Communication in Integrated Networks of Resistance Arteries
Author(s) -
Tunuguntla Jaya Deep,
Vigmond Edward J,
Welsh Donald Gordon
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a522-a
Subject(s) - resistor , gap junction , artery , hyperpolarization (physics) , anatomy , conductance , chemistry , neuroscience , biomedical engineering , medicine , cardiology , biology , physics , voltage , electrical engineering , engineering , biochemistry , organic chemistry , condensed matter physics , nuclear magnetic resonance spectroscopy , intracellular
Vascular cells within arterial networks electrically communicate with one another to control tissue blood flow. To ascertain how charge distributes within an arterial network, we extended an existing model of electrical communication so that virtual arteries of variable dimension could be connected to one another. In general, each virtual artery consisted of one layer of endothelium and a single layer of smooth muscle. Each vascular cell was treated as the electrical equivalent of capacitor coupled in parallel with a non‐linear voltage dependent resistor (representing ionic conductance). Gap junctions interconnected neighboring cells and were represented as ohmic resistors. Simulations revealed that hyperpolarization initiated in a small number of endothelial cells spreads with little decay along an arterial wall. As these endothelial‐initiated responses conducted across a branch point, electrical decay was enhanced. The extent of decay varied according to the relative diameter of the daughter and parent arteries. Computational observations coincided with functional observations of cell‐to‐cell communication in the mouse cremaster preparation. Further simulations revealed the ability of electrical responses initiated in two daughter vessels to summate in a parent vessel and for hyperpolarizing stimuli originating in multiple distal vessels to dilate large proximal arteries. Together, these observations begin to highlight how the structural features of an arterial network influence cell‐to‐cell communication. These findings have important functional implications to the hyperemic response in normal and diseased animals. Funded by AHFMR and HSFC.