Conducted depolarization in arteriole networks of the guinea-pig small intestine: effect of branching of signal dissipation.
1. Blood flow control requires co-ordinated activity among many branches of arteriole networks, which may be achieved by conduction of membrane potential changes between arteriolar smooth muscle cells and endothelial cells. 2. We investigated the effect of branching upon the passive conduction of electrical signals through the syncytium of electrically coupled cells in arteriole networks (n = 12) prepared from the guinea-pig submucosa. To describe the effect of branching on cable properties, the expansion parameter B was calculated (B = 1 for an unbranched cable; B > 1 with branching) for a point in each arteriole network based on anatomy. 3. An estimate of B(B') was also obtained by measuring the spread of depolarization caused by a high-K+ stimulus applied to one region. Membrane potential (-74 +/- 4 mV (+/- S.D.) at rest) was recorded from smooth muscle cells (verified with intracellular dye labelling). A micropipette containing 120 mM KCl was positioned at 150 micron increments along an arteriole (width, 50-75 microns) up to approximately 1.2 mm from a stationary recording site, producing stable depolarization which decreased as separation distance increased. The dissipation of depolarization with separation was greater when recording near branch origins rather than continuous segments. 4. B ranged in value from 0.99 to 2.28. In any one experiment, values of B and B' were correlated (correlation coefficient, r = 0.71; P < 0.05), but B' was consistently greater than B, and we discuss methodological factors which could lead to erroneously high values for B'. 5. For pooled electrophysiological data, depolarization decayed to 37% (1/e) of initial values in approximately 700 microns, consistent with B > 1. In contrast, the conduction of vasoconstriction and vasodilatation exceeds 2 mm in arteriole networks in previous studies. To explain this discrepancy, we suggest that active electrical events in cells of the arteriole wall augment passive electrical conduction during blood flow control.
Segal
S S
SS
Department of Human Physiology, Flinders University, Adelaide, Australia. SSSegal@aol.com
Neild
T O
TO
D000818:Animals; D001160:Arterioles / Q000033:anatomy & histology / Q000294:innervation / Q000502:physiology; D004558:Electric Stimulation; D004594:Electrophysiology; D005260:Female; D005456:Fluorescent Dyes; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000187:drug effects / Q000502:physiology; D007421:Intestine, Small / Q000098:blood supply / Q000294:innervation* / Q000502:physiology; D007546:Isoquinolines; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000494:pharmacology; D012039:Regional Blood Flow / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D005456:Fluorescent Dyes; D007546:Isoquinolines; C017475:lucifer yellow; D011188:Potassium