The effect of intracellular cyclic nucleotides and calcium on the action potential and acetylcholine response of isolated cardiac cells

1982 ◽  
Vol 392 (4) ◽  
pp. 307-314 ◽  
Author(s):  
W. Trautwein ◽  
J. Taniguchi ◽  
A. Noma
Keyword(s):  
Action Potential ◽  
Cyclic Nucleotides ◽  
Cardiac Cells ◽  
Isolated Cardiac Cells

Electrophysiology of the Sodium-Potassium-ATPase in Cardiac Cells

2001 ◽  
Vol 81 (4) ◽  
pp. 1791-1826 ◽  
Author(s):  
Helfried Günther Glitsch
Keyword(s):  
Cell Membrane ◽  
Potential Gradient ◽  
Outward Current ◽  
Pump Current ◽  
Cardiac Cells ◽  
Animal Cells ◽  
Excitable Cells ◽  
Extracellular Medium ◽  
Enzymatic Isolation ◽  
Isolated Cardiac Cells

Like several other ion transporters, the Na+-K+ pump of animal cells is electrogenic. The pump generates the pump current I p. Under physiological conditions, I p is an outward current. It can be measured by electrophysiological methods. These methods permit the study of characteristics of the Na+-K+ pump in its physiological environment, i.e., in the cell membrane. The cell membrane, across which a potential gradient exists, separates the cytosol and extracellular medium, which have distinctly different ionic compositions. The introduction of the patch-clamp techniques and the enzymatic isolation of cells have facilitated the investigation of I p in single cardiac myocytes. This review summarizes and discusses the results obtained from I p measurements in isolated cardiac cells. These results offer new exciting insights into the voltage and ionic dependence of the Na+-K+ pump activity, its effect on membrane potential, and its modulation by hormones, transmitters, and drugs. They are fundamental for our current understanding of Na+-K+ pumping in electrically excitable cells.

scholarly journals Calcium sensitivity of the contractile system and phosphorylation of troponin in hyperpermeable cardiac cells.

1980 ◽  
Vol 75 (3) ◽  
pp. 271-282 ◽  
Author(s):  
L Mope ◽  
G B McClellan ◽  
S Winegrad
Keyword(s):  
Cyclic Nucleotides ◽  
Polyacrylamide Gel Electrophoresis ◽  
Calcium Sensitivity ◽  
Ventricular Myocardium ◽  
Cardiac Cells ◽  
Contractile System ◽  
Maximum Activation ◽  
Nonionic Detergent ◽  
Inhibitory Subunit Of Troponin ◽  
Ca Sensitivity

Bundles of cells from rat right ventricular myocardium were made "hyperpermeable" by an overnight soak in 10 mM EGTA (McClellan and Winegrad. 1978. J. Gen. Physiol. 72:737-764). In this preparation the cytoplasmic concentration of Ca++ and ATP could be controlled while sarcolemmal receptors and enzymes were retained. The Ca sensitivity of the tissues (as indicated by the pCa for 50% maximum activation) was altered to different extents in the presence of [32Pgamma]ATP by treatment with cyclic nucleotides, catecholamines, or a low concentration of nonionic detergent. The proteins of the tissue were then isolated by SDS-polyacrylamide gel electrophoresis, and the identity of 32P-labeled proteins was determined. The Ca sensitivity is inversely related to the relative amount of 32P incorporated into the inhibitory subunit of troponin (TNI). Extrapolation of the relation to the lowest Ca sensitivity observed gives a stoichiometry of about 0.8 mol PO4 per mol TNI. These results support the hypothesis that Ca sensitivity of cardiac myofibrils is regulated by a phosphrylation of TNI that is stimulated by cyclic AMP (cAMP) and inhibited by cGMP.

Mechanisms and Physiological Implications of Cooperative Gating of Ion Channels Clusters

2021 ◽  
Author(s):  
Rose Ellen Dixon ◽  
Manuel F. Navedo ◽  
Marc D Binder ◽  
L. Fernando Santana
Keyword(s):  
Ion Channels ◽  
Action Potential ◽  
Transient Receptor Potential ◽  
Imaging Techniques ◽  
Ryanodine Receptors ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Cardiac Cells ◽  
Fine Tuning ◽  
Voltage Gated

Ion channels play a central role in the regulation of nearly every cellular process. Dating back to the classic 1952 Hodgkin-Huxley model of the generation of the action potential, ion channels have always been thought of as independent agents. A myriad of recent experimental findings exploiting advances in electrophysiology, structural biology, and imaging techniques, however, have posed a serious challenge to this long-held axiom as several classes of ion channels appear to open and close in a coordinated, cooperative manner. Ion channel cooperativity ranges from variable-sized oligomeric cooperative gating in voltage-gated, dihydropyridine-sensitive Cav1.2 and Cav1.3 channels to obligatory dimeric assembly and gating of voltage-gated Nav1.5 channels. Potassium channels, transient receptor potential channels, hyperpolarization cyclic nucleotide-activated channels, ryanodine receptors (RyRs), and inositol trisphosphate receptors (IP3Rs) have also been shown to gate cooperatively. The implications of cooperative gating of these ion channels range from fine tuning excitation-contraction coupling in muscle cells to regulating cardiac function and vascular tone, to modulation of action potential and conduction velocity in neurons and cardiac cells, and to control of pace-making activity in the heart. In this review, we discuss the mechanisms leading to cooperative gating of ion channels, their physiological consequences and how alterations in cooperative gating of ion channels may induce a range of clinically significant pathologies.

Electrophysiological heterogeneity and stability of reentry in simulated cardiac tissue

2001 ◽  
Vol 280 (2) ◽  
pp. H535-H545 ◽  
Author(s):  
Fagen Xie ◽  
Zhilin Qu ◽  
Alan Garfinkel ◽  
James N. Weiss
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Cardiac Tissue ◽  
Potential Model ◽  
Dynamic Instability ◽  
Spatial Scales ◽  
Cardiac Cells ◽  
Dynamic Factors ◽  
Cardiac Model ◽  
Wave Break

Generation of wave break is a characteristic feature of cardiac fibrillation. In this study, we investigated how dynamic factors and fixed electrophysiological heterogeneity interact to promote wave break in simulated two-dimensional cardiac tissue, by using the Luo-Rudy (LR1) ventricular action potential model. The degree of dynamic instability of the action potential model was controlled by varying the maximal amplitude of the slow inward Ca2+ current to produce spiral waves in homogeneous tissue that were either nearly stable, meandering, hypermeandering, or in breakup regimes. Fixed electrophysiological heterogeneity was modeled by randomly varying action potential duration over different spatial scales to create dispersion of refractoriness. We found that the degree of dispersion of refractoriness required to induce wave break decreased markedly as dynamic instability of the cardiac model increased. These findings suggest that reducing the dynamic instability of cardiac cells by interventions, such as decreasing the steepness of action potential duration restitution, may still have merit as an antifibrillatory strategy.

scholarly journals Theoretical Aspects of Resting-State Cardiomyocyte Communication for Multi-Nodal Nano-Actuator Pacemakers

Sensors ◽  
2020 ◽  
Vol 20 (10) ◽  
pp. 2792
Author(s):  
Pengfei Lu ◽  
Mladen Veletić ◽  
Jacob Bergsland ◽  
Ilangko Balasingham
Keyword(s):  
Action Potential ◽  
Resting State ◽  
Communication Channel ◽  
Potential Model ◽  
Signal Propagation ◽  
Cardiac Cells ◽  
The Body ◽  
Cardiac Muscle Cells ◽  
Leadless Pacemaker ◽  
Communication Technique

The heart consists of billions of cardiac muscle cells—cardiomyocytes—that work in a coordinated fashion to supply oxygen and nutrients to the body. Inter-connected specialized cardiomyocytes form signaling channels through which the electrical signals are propagated throughout the heart, controlling the heart’s beat to beat function of the other cardiac cells. In this paper, we study to what extent it is possible to use ordinary cardiomyocytes as communication channels between components of a recently proposed multi-nodal leadless pacemaker, to transmit data encoded in subthreshold membrane potentials. We analyze signal propagation in the cardiac infrastructure considering noise in the communication channel by performing numerical simulations based on the Luo-Rudy computational model. The Luo-Rudy model is an action potential model but describes the potential changes with time including membrane potential and action potential stages, separated by the thresholding mechanism. Demonstrating system performance, we show that cardiomyocytes can be used to establish an artificial communication system where data are reliably transmitted between 10 s of cells. The proposed subthreshold cardiac communication lays the foundation for a new intra-cardiac communication technique.

Development of a linear transient model for stimulation of isolated cardiac cells

2000 ◽  
Vol 12 (3) ◽  
pp. 217-222 ◽  
Author(s):  
P. Pham ◽  
G. Cauffet ◽  
A. Bardou ◽  
J. Olivares ◽  
E. Novakov
Keyword(s):  
Cardiac Cells ◽  
Transient Model ◽  
Isolated Cardiac Cells ◽  
Stimulation Of

Cyclic nucleotides in spinal cells

1976 ◽  
Vol 54 (3) ◽  
pp. 416-421 ◽  
Author(s):  
K. Krnjevic ◽  
W. G. Van Meter
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cyclic Nucleotides ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Cyclic Monophosphate ◽  
Synaptic Facilitation ◽  
Marked Enhancement

The most striking effects of intracellular injections of adenosine 3′5′-cyclic monophosphate (cAMP) into spinal mononeurons in cats are a speeding-up of the action potential, both its rising and falling phase, and a potentiation of the after-hyperpolarization; the latter probably indicates a marked enhancement of Ca2+ influx. In this respect, cAMP and guanosine 3′5′-cyclic monophosphate (cGMP) have similar actions, though cAMP appears to be more potent. It is suggested that through this mechanism, cyclic nucleotides may play an important role in synaptic facilitation. Changes in resting membrane potential and resistance are less conspicuous or predictable. By contrast, both agents, when injected into unresponsive cells, presumed to be neuroglia, regularly cause a drop in membrane resistance; this is associated with hyperpolarization and therefore likely to reflect an increase in membrane K+ conductance.

Junctional Sarcoplasmic Reticulum in Excitation-Contraction-Coupling

1982 ◽  
Vol 40 ◽  
pp. 136-137
Author(s):  
J.R. Sommer ◽  
E. Bossen ◽  
A. Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Contraction ◽  
Cardiac Cells ◽  
Close Apposition ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Terminal Cisterna ◽  
Voltage Dependent ◽  
Junctional Sarcoplasmic Reticulum

The junctional sarcoplasmic reticulum (JSR, syn. terminal cisterna) is implicated in Ca++storage and release for muscle contraction. Its discrete ultrastructure permits distinction from the rest of the SR (free SR) even when it occurs without plasmalemmal contact, e.g. as extended JSR (EJSR) in bird, and corbular SR (CSR) in mammalian cardiac cells. The close apposition of JSR to plasmalemma via junctional processes is central to proposed mechanisms of translating voltage-dependent charge transfers at the plasmalemma during the action potential into Ca++release from the JSR. These hypotheses are put into question by the existence of EJSR (and CSR) which in birds constitutes 70-80% of the total JSR. An alternate hypothesis proposes, at least for cardiac cells, that Ca++entering the cell during excitation causes additional Ca++to be freed intracellularly. The notion of a chemical transmitter acting by diffusion is attractive because it will allow for the anomalous topography of EJSR, especially since bird cardiac cells have only about half the diameter of their mammalian relatives and have no transverse tubules.

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