Electrotonic modulation of electrical activity in rabbit atrioventricular node myocytes

1997 ◽  
Vol 273 (2) ◽  
pp. H767-H776 ◽  
Author(s):  
K. W. Spitzer ◽  
N. Sato ◽  
H. Tanaka ◽  
L. Firek ◽  
M. Zaniboni ◽  
...  

Electrotonic effects of electrically coupling atrioventricular (AV) nodal cells to each other and to real and passive models of atrial and ventricular cells were studied using a technique that does not require functional gap junctions. Membrane potential was measured in each cell using suction pipettes. Mutual entrainment of two spontaneously firing AV nodal cells was achieved with a junctional resistance (Rj) of 500 M omega, which corresponds to only 39 junctional channels, assuming a single-channel conductance of 50 pS. Coupling of AV nodal and atrial cells at Rj of 50 M omega caused hyperpolarization of the nodal cell, decreasing its action potential duration and either slowing or blocking diastolic depolarization in the AV node myocyte. Opposite changes occurred in the atrial action potential. When AV nodal and ventricular cells were coupled at Rj of 50 M omega, nodal diastolic potential was markedly hyperpolarized and diastolic depolarization was completely blocked with little change in ventricular diastolic potential. However, coupling did elicit marked changes in the action potential duration of both cells, with prolongation in the nodal cell and shortening in the ventricular cell. Nodal maximum upstroke velocity was increased by both atrial and ventricular coupling, as expected from the hyperpolarization that occurred. With an Rj of 50 M omega, spontaneous firing was blocked in all single AV nodal pacemaker cells during coupling to a real or passive model of an atrial or ventricular cell. These results demonstrate that action potential formation and waveform in a single AV nodal cell is significantly affected by electrical coupling to other myocytes.

1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.


1989 ◽  
Vol 256 (2) ◽  
pp. C452-C455 ◽  
Author(s):  
Z. S. Agus ◽  
E. Kelepouris ◽  
I. Dukes ◽  
M. Morad

The effect of cytosolic free Mg2+ concentration on the regulation of myocardial function was studied by dialyzing isolated guinea pig ventricular myocytes with different internal Mg2+ concentrations [( Mg2+]i). We found that elevation of [Mg2+]i shortened the action potential and suppressed the Ca2+ current. Mean values recorded for action potential duration in cells dialyzed with solutions containing 0, 1.3, and 9.4 mM Mg2+ were 620 +/- 40, 400 +/- 25, and 60 +/- 10, respectively. The suppressive effect of [Mg2+]i on the action potential duration correlated significantly with the suppressive effects of [Mg2+]i on the Ca2+ current. In cells dialyzed with nominally zero Mg2+, calcium current was prominent (3.5 +/- 0.58 nA). At [Mg2+]i of 1.4 mM, calcium current was significantly smaller than in zero [Mg2+]i and was almost completely inhibited by dialysis of the cell with 9.4 mM Mg2+. The Mg2+-induced block of the Ca2+ current was due to steady-state inactivation of the high threshold calcium channel. The block was observed in the presence or absence of adenosine 3',5'-cylic monophosphate and was not reversed by elevation of external Ca2+ concentration, addition of adrenaline, or large negative potentials. These data suggest that cytosolic Mg2+ regulates Ca2+ channel activity by a novel mechanism, unrelated to its effect as a blocking particle of the open channel.


2010 ◽  
Vol 31 (6) ◽  
pp. 413-417 ◽  
Author(s):  
Shintaro Yamamoto ◽  
Takuya Iyoda ◽  
Satomi Kita ◽  
Toshiki Yamada ◽  
Takahiro Iwamoto

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
S. H. Sabzpoushan ◽  
A. Ghajarjazy

Ventricular action potential is well-known because of its plateau phase with a spike-notch-dome morphology. As such, the morphology of action potential is necessary for ensuring a correct heart functioning. Any distraction from normal notch-dome morphology may trigger a circus movement reentry in the form of lethal ventricular fibrillation. When the epicardial action potential dome propagates from a site where it is maintained to regions where it has been lost, it gives rise to the proposed mechanism for the Brugada syndrome. Despite the impact of notch-dome dynamics on the heart function, no independent and explicit research has been performed on the simulation of notch-dome dynamics and morphology. In this paper, using a novel mathematical approach, a three-state variable model is proposed; we show that our proposed model not only can simulate morphology of action potential of ventricular cells but also can propose a biological reasonable tool for controlling of the morphology of action potential spike-notch-dome. We show that the processes of activation and inactivation of ionic gating variables (as positive or negative feedbacks on the voltage of cell membrane) and the ratio of their speeds (time constants) can be treated as a reasonable biological tool for simulating ventricular cell notch-dome. This finding may led to a new insight to the quantification of the health of a ventricular cell and may also propose a new drug therapy strategy for cardiac diseases.


1998 ◽  
Vol 111 (1) ◽  
pp. 95-112 ◽  
Author(s):  
E. Etienne Verheijck ◽  
Ronald Wilders ◽  
Ronald W. Joyner ◽  
David A. Golod ◽  
Rajiv Kumar ◽  
...  

The effects of intercellular coupling conductance on the activity of two electrically coupled isolated rabbit sinoatrial nodal cells were investigated. A computer-controlled version of the “coupling clamp” technique was used in which isolated sinoatrial nodal cells, not physically in contact with each other, were electrically coupled at various values of ohmic coupling conductance, mimicking the effects of mutual interaction by electrical coupling through gap junctional channels. We demonstrate the existence of four types of electrical behavior of coupled spontaneously active cells. As the coupling conductance is progressively increased, the cells exhibit: (a) independent pacemaking at low coupling conductances, (b) complex dynamics of activity with mutual interactions, (c) entrainment of action potential frequency at a 1:1 ratio with different action potential waveforms, and (d) entrainment of action potentials at the same frequency of activation and virtually identical action potential waveforms. The critical value of coupling conductance required for 1:1 frequency entrainment was <0.5 nS in each of the five cell pairs studied. The common interbeat interval at a relatively high coupling conductance (10 nS), which is sufficient to produce entrainment of frequency and also identical action potential waveforms, is determined most by the intrinsically faster pacemaker cell and it can be predicted from the diastolic depolarization times of both cells. Evidence is provided that, at low coupling conductances, mutual pacemaker synchronization results mainly from the phase-resetting effects of the action potential of one cell on the depolarization phase of the other. At high coupling conductances, the tonic, diastolic interactions become more important.


1980 ◽  
Vol 58 (4) ◽  
pp. 433-435 ◽  
Author(s):  
M. D. Payet ◽  
G. Bkaily ◽  
O. F. Schanne ◽  
E. Ruiz-Ceretti

In clusters of trypsinized ventricle cells from neonatal rats which exhibit slow response action potentials, streptomycin in concentrations from 0.17 to 5.5 mM significantly inhibits the beating rate. Microelectrode experiments performed at a concentration of 5.5 mM revealed a reduction in the slope of diastolic depolarization from 149 to 53 mV/s whereas the maximum diastolic potential depolarized from −42.4 to −33.6 mV which entailed a decrease in overshoot and maximum rate of rise of the action potential. We conclude that the decrease of the slope of diastolic depolarization mainly determines the slowing of the beating rate and that streptomycin interferes with the pacemaker mechanism usually associated with the slow response.


1987 ◽  
Vol 7 (3) ◽  
pp. 148-152
Author(s):  
Tang Ming ◽  
Zhang Guang-lan ◽  
Zeng Xiao-rong ◽  
Zhong Jun-yuan ◽  
Zhang Yi ◽  
...  

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