Simulation of the electrocardiographic U wave in heterogeneous myocardium: effect of local junctional resistance

2003 ◽  
Author(s):  
V.V. Nesterenko ◽  
C. Antzelevitch
Keyword(s):  
Junctional Resistance

scholarly journals Changes in Tight Junctional Resistance of the Cervical Epithelium Are Associated with Modulation of Content and Phosphorylation of Occludin 65-Kilodalton and 50-Kilodalton Forms

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 977-989 ◽  
Author(s):  
Ling Zhu ◽  
Xin Li ◽  
Robin Zeng ◽  
George I. Gorodeski
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tight Junction ◽  
Tyrosine Phosphorylation ◽  
Tight Junctions ◽  
Early Stage ◽  
Cervical Epithelium ◽  
Kinase C ◽  
Low Levels ◽  
Junctional Resistance

Treatment of human cervical epithelial CaSki cells with ATP or with the diacylglyceride sn-1,2-dioctanoyl diglyceride (diC8) induced a staurosporine-sensitive transient increase, followed by a late decrease, in tight-junctional resistance (RTJ). CaSki cells express two immunoreactive forms of occludin, 65 and 50 kDa. Treatments with ATP and diC8 decreased the density of the 65-kDa form and increased the density of the 50-kDa form. ATP also decreased threonine phosphorylation of the 65-kDa form and increased threonine phosphorylation of the 50-kDa form and tyrosine phosphorylation of the 65- and 50-kDa forms. Staurosporine decreased acutely threonine and tyrosine phosphorylation of the two isoforms and in cells pretreated with staurosporine ATP increased acutely the density of the 65-kDa form and threonine phosphorylation of the 65-kDa form. Treatment with N-acetyl-leucinyl-leucinyl-norleucinal increased the densities of the 65- and 50-kDa forms. Pretreatment with N-acetyl-leucinyl-leucinyl-norleucinal attenuated the late decreases in RTJ induced by ATP and diC8 and the decrease in the 65-kDa and increase in the 50-kDa forms induced by ATP. Correlation analyses showed that high levels of RTJ correlated with the 65-kDa form, whereas low levels of RTJ correlated negatively with the 65-kDa form and positively with the 50-kDa form. The results suggest that in CaSki cells 1) occludin determines gating of the tight junctions, 2) changes in occludin phosphorylation status and composition regulate the RTJ, 3) protein kinase-C-mediated, threonine dephosphorylation of the 65-kDa occludin form increases the resistance of assembled tight junctions, 4) the early stage of tight junction disassembly involves calpain-mediated breakdown of occludin 65-kDa form to the 50-kDa form, and 5) increased levels of the 50-kDa form interfere with occludin gating of the tight junctions.

Effects of octanol on canine subendocardial Purkinje-to-ventricular transmission

1985 ◽  
Vol 249 (6) ◽  
pp. H1228-H1231 ◽  
Author(s):  
R. W. Joyner ◽  
E. D. Overholt
Keyword(s):  
Action Potential ◽  
Conduction Velocity ◽  
Current Flow ◽  
Conduction Delay ◽  
Papillary Muscles ◽  
Maximal Rate ◽  
Gap Junctional ◽  
Junctional Resistance ◽  
P Cells

The effects of 0.2 mM octanol on action potential propagation were investigated using in vitro preparations of canine papillary muscles. In these preparations an action potential initiated in the superficial Purkinje (P) layer propagates across specific Purkinje-ventricular junction (PVJ) sites into the underlying ventricular (V) layer. The conduction delay at PVJ sites increased from 4.85 +/- 1.55 to 8.85 +/- 3.34 (mean +/- SD) ms (n = 10, P less than 0.005), an 82% increase. However, propagation within the V syncytium was much less affected, with a decrease of conduction velocity by only 10% and a decrease in the maximal rate of rise of the action potential of 23%. The results indicate that octanol, which has previously been shown to increase gap junctional resistance, has a preferential effect on PVJ sites, as predicted by the hypothesis that there is a restricted pathway for intracellular current flow from P cells to V cells at these sites.

Two classes of tight junctions are revealed by ZO-1 isoforms

1993 ◽  
Vol 264 (4) ◽  
pp. C918-C924 ◽  
Author(s):  
M. S. Balda ◽  
J. M. Anderson
Keyword(s):  
Tight Junction ◽  
Tight Junctions ◽  
Rna Splicing ◽  
Seminiferous Tubules ◽  
Junction Protein ◽  
Acid Domain ◽  
Ribonuclease Protection ◽  
Tissue Compartments ◽  
Junctional Resistance ◽  
Amino Acid Domain

The tight junction forms the intercellular barrier separating tissue compartments. The characteristics of this barrier are remarkably diverse among different epithelia and endothelia and are not explained by our limited knowledge of its molecular composition. Two isoforms of the 220-kDa tight junction protein ZO-1 result from alternative RNA splicing and differ by an internal 80-amino acid domain, termed alpha (E. Willott, M. S. Balda, M. Heintzman, B. Jameson, and J. M. Anderson. Am. J. Physiol. 262 (Cell Physiol. 31): C1119-C1124, 1992). Using antibodies specific for each isoform and double-labeled immunofluorescence microscopy, we observed that the ZO-1 alpha- isoform is restricted to junctions of endothelial cells and highly specialized epithelial cells of both seminiferous tubules (Sertoli cells) and renal glomeruli (podocytes); in contrast, the ZO-1 alpha+ isoform is expressed in cells of all other epithelia examined. Both immunoblotting and ribonuclease protection analysis confirmed this pattern of expression. This distribution does not correlate with differences in junctional resistance or ultrastructural complexity. Instead, we observe a correlation with junctional plasticity; ZO-1 alpha- is expressed in structurally dynamic junctions, whereas ZO-1 alpha+ is expressed in those which are less dynamic. This is the first molecular distinction among tight junctions and reveals a fundamental dichotomy with implications for how the paracellular barriers of endothelia and epithelia are regulated.

Extracellular ATP regulates transcervical permeability by modulating two distinct paracellular pathways

1997 ◽  
Vol 272 (5) ◽  
pp. C1602-C1610 ◽  
Author(s):  
G. I. Gorodeski ◽  
J. Goldfarb
Keyword(s):  
Phase I ◽  
Phase Ii ◽  
Extracellular Atp ◽  
Acetoxymethyl Ester ◽  
Experimental Conditions ◽  
Mucus Production ◽  
Atp Regulation ◽  
Junctional Resistance ◽  
Kinetics Of

Extracellular ATP stimulates a biphasic change in transepithelial electrical resistance (RTE) across cultures of human cervical epithelial cells: an acute decrease (phase I), followed by a delayed increase in resistance (phase II). The objective of this study was to determine the contributions of changes in the lateral intercellular space resistance (RLIS) and the tight junctional resistance (RTJ) to the changes in RTE. Phase I and phase II effects were uncoupled by treatment with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA)-acetoxymethyl ester, which blocks the ATP-induced increases in cytosolic Ca2+ and abolishes phase I. BAPTA-loaded cells differed from control cells in that 1) phase I began when ATP was added, in contrast to a delay of 1.5-3.5 min in phase II, 2) phase I decreases in RLIS followed a simple exponential pattern, in contrast to the complex kinetics of phase II, and 3) the magnitude of phase II varied between 20 and 100% for increases of RTJ in day 2-6 cultures; the phase I decrease of 50% in RLIS was unrelated to different experimental conditions. These results indicate that phase I and phase II are induced simultaneously and independently by ATP, and they contribute to the total changes in RTE. We conclude that ATP regulation of RLIS and RTJ may be important mechanisms of modulating cervical mucus production in vivo.

Some bio-electric parameters of early Xenopus embryos

Development ◽  
1970 ◽  
Vol 24 (3) ◽  
pp. 535-553
Author(s):  
J. F. Palmer ◽  
Christine Slack
Keyword(s):  
Membrane Potential ◽  
South African ◽  
Developmental Stages ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Mean Value ◽  
Cell Junctions ◽  
Current Spread ◽  
Intracellular Microelectrodes ◽  
Junctional Resistance

Membrane potential and resistance were measured in eggs, cleavage stages and blastulae of the South African toad Xenopus laevis, using intracellular microelectrodes. The membrane potential increased from −6·5 ± 2mV in eggs to −57 ± 8·0mV at the mid-blastula stage. The input resistance of fertile eggs ranged from 0·5 MΩ to 5·0 MΩ corresponding to a specific resistance of 20–200kΩcm2. During the first two or three division cycles the input resistance usually decreased by a factor of 2–10 and then subsequently rose during the blastula stages from a mean value of 600 ± 100kΩ at stage 5 to 2·0 ± 0·5 MΩ at stage 8. At all developmental stages examined, point polarization of a surface cell in the embryo by rectangular current pulses of 0·5−6 × 10−8 A produced voltage deflexions in other surface cells. This was seen even when several (7–8) cell junctions intervened between the current passing and voltage recording microelectrodes at distances of more than 1 mm. These measurements suggest that the junctional resistance is low compared with that at the surface, though the geometrical arrangement of cells is not favourable for calculation of absolute values of membrane resistance. Current spread between cells occurred apparently less easily during mid-blastula stages than at earlier stages in development, perhaps indicating an increase in junctional resistance during development. A comparison has been drawn between the present measurements and similar ones made in another amphibian, Triturus.

Modulation of repolarization in rabbit Purkinje and ventricular myocytes coupled by a variable resistance

1999 ◽  
Vol 276 (2) ◽  
pp. H572-H581 ◽  
Author(s):  
Delilah J. Huelsing ◽  
Kenneth W. Spitzer ◽  
Jonathan M. Cordeiro ◽  
Andrew E. Pollard
Keyword(s):  
Action Potential ◽  
Computer Simulations ◽  
Calcium Current ◽  
Electronic Circuit ◽  
Ventricular Myocytes ◽  
Phase 1 ◽  
Inward Rectifier ◽  
The Difference ◽  
Coupling Current ◽  
Junctional Resistance

Purkinje-ventricular junctions (PVJs) have been implicated as potential sites of arrhythmogenesis, in part because of the dispersion of action potential duration (APD) between Purkinje (P) and ventricular (V) myocytes. To characterize electrotonic modulation of APD as a function of junctional resistance ( R j), we coupled single isolated rabbit P and V myocytes with an electronic circuit. In seven of eight PV myocyte pairs, both APDs shortened on coupling at R j = 50 MΩ. This was in contrast to modulation of APD in paired ventricular myocytes, which demonstrated APD shortening of the intrinsically longer action potential and APD prolongation of the intrinsically shorter action potential. Companion computer simulations, performed to suggest possible mechanisms for the paradoxical shortening of the V action potential in paired P and V myocytes, showed that the difference in intrinsic peak plateau potentials ( V pp) of the P and V myocytes determined whether the V action potential shortened or prolonged on coupling. This difference in V pp caused a large, repolarizing coupling current to flow to the V myocyte, contributing to early inactivation of the L-type calcium current and early activation of the inward rectifier current. These results suggest that intrinsic differences in phase 1 repolarization could yield differing patterns of APD shortening or prolongation in the network of subendocardial PVJs, leaving some PVJs vulnerable to conduction of premature stimuli while other PVJs remain refractory.

Conduction between isolated rabbit Purkinje and ventricular myocytes coupled by a variable resistance

1998 ◽  
Vol 274 (4) ◽  
pp. H1163-H1173 ◽  
Author(s):  
Delilah J. Huelsing ◽  
Kenneth W. Spitzer ◽  
Jonathan M. Cordeiro ◽  
Andrew E. Pollard
Keyword(s):  
Electronic Circuit ◽  
Ventricular Myocytes ◽  
Phase 1 ◽  
Conduction Block ◽  
Outward Current ◽  
Transient Outward Current ◽  
Electrotonic Interactions ◽  
Unidirectional Block ◽  
The Mean ◽  
Junctional Resistance

Conduction at the Purkinje-ventricular junction (PVJ) demonstrates unidirectional block under both physiological and pathophysiological conditions. Although this block is typically attributed to multidimensional electrotonic interactions, we examined possible membrane-level contributions using single, isolated rabbit Purkinje (P) and ventricular (V) myocytes coupled by an electronic circuit. When we varied the junctional resistance ( R j) between paired V myocytes, conduction block occurred at lower R j values during conduction from the smaller to larger myocyte (115 ± 59 MΩ) than from the larger to smaller myocyte (201 ± 51 MΩ). In Purkinje-ventricular myocyte pairs, however, block occurred at lower R j values during P-to-V conduction (85 ± 39 MΩ) than during V-to-P conduction (912 ± 175 MΩ), although there was little difference in the mean cell size. Companion computer simulations, performed to examine how the early plateau currents affected conduction, showed that P-to-V block occurred at lower R j values when the transient outward current was increased or the calcium current was decreased in the model P cell. These results suggest that intrinsic differences in phase 1 repolarization can contribute to unidirectional block at the PVJ.

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