scholarly journals The control of tonic tension by membrane potential and intracellular sodium activity in the sheep cardiac Purkinje fibre.

1983 ◽  
Vol 335 (1) ◽  
pp. 723-743 ◽  
Author(s):  
D A Eisner ◽  
W J Lederer ◽  
R D Vaughan-Jones
Keyword(s):  
Membrane Potential ◽  
Intracellular Sodium ◽  
Purkinje Fibre ◽  
Sodium Activity ◽  
Cardiac Purkinje Fibre ◽  
Tonic Tension

The interrelationship of cesium, intracellular sodium activity, and pacemaker potential in cardiac Purkinje fibers

1990 ◽  
Vol 68 (9) ◽  
pp. 1236-1246 ◽  
Author(s):  
Giovanni Iacono ◽  
Mario Vassalle
Keyword(s):  
Membrane Potential ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Sodium Activity ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Myocardial Fibers

The actions of cesium (Cs) on intracellular sodium activity [Formula: see text], membrane potentials, and force were studied in sheep cardiac Purkinje and myocardial fibers superfused in vitro. In Purkinje fibers, Cs (2 mM) decreased diastolic depolarization, [Formula: see text] (−6.7%, p < 0.005), and force (−28.0%, p < 0.01). The effects of 4 and 8 mM Cs were more pronounced. In quiescent fibers, Cs (2–4 mM) also decreased [Formula: see text] (−17.3%, p < 0.005) and induced an initial hyperpolarization (+5.6 ± 1.3%, p < 0.005) followed by a return toward control. Diastolic depolarization was almost abolished by driving the fibers at 180/min (diastole was very short) but still Cs decreased [Formula: see text] (−15.4%). Tetrodotoxin decreased [Formula: see text] (−16.2%, p < 0.025) and reduced the Cs-induced fall in [Formula: see text] (−2.2%, p < 0.05). In zero [K]o, Cs decreased [Formula: see text] and caused repolarization. In 0.1 mM strophanthidin, Cs did not decrease [Formula: see text] any longer and affected the membrane potential little. In quiescent myocardial fibers, Cs (4 mM) decreased [Formula: see text] (−12.6%, p < 0.05) and transiently hyperpolarized (+2.1%). Rubidium (2 mM) decreased [Formula: see text] and resting potential in Purkinje fibers and in myocardial fibers and also decreased diastolic depolarization in Purkinje fibers. Thus, cesium and rubidium decrease [Formula: see text] and modify the membrane potential but not through a block of the inward pacemaker current If.Key words: rubidium, intracellular sodium activity, diastolic depolarization, tetrodotoxin, strophanthidin.

Cellular and subcellular mechanisms of cardiac pacemaker oscillations

1979 ◽  
Vol 81 (1) ◽  
pp. 205-215
Author(s):  
R. W. Tsien ◽  
R. S. Kass ◽  
R. Weingart
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Surface Membrane ◽  
Cardiac Pacemaker ◽  
Oscillatory Activity ◽  
Purkinje Fibre ◽  
Pacemaker Activity ◽  
Heart Cells ◽  
Control Loop ◽  
Internal Oscillation

Rhythmic oscillations in the membrane potential of heart cells are important in normal cardiac pacemaker activity as well as cardiac arrhythmias. Two fundamentally different mechanisms of oscillatory activity can be distinguished at the cellular and subcellular level. The first mechanism, referred to as a surface membrane oscillator, can be represented by a control loop in which membrane potential changes evoke delayed conductance changes and vice versa. Since the surface membrane potential is a key variable within the control loop, the oscillation can be interrupted at any time by holding the membrane potential constant with a voltage clamp. This mode of oscillation seems to describe spontaneous pacemaker activity in the primary cardiac pacemaker (sinoatrial node) as well as other regions (Purkinje fibre, atrial or ventricular muscle). In all tissues studied so far, the pacemaker depolarization is dominated by the slow shutting-off of an outward current, largely carried by potassium ions. The second mechanism can be called an internal oscillator since it depends upon a subcellular rhythm generator which is largely independent from the surface membrane. Under voltage clamp, the existence of the internal oscillation is revealed by the presence of oscillations in membrane conductance or contractile force which occur even though the membrane potential is held fixed. The two oscillatory mechanisms are not mutually exclusive; the subcellular mechanism can be preferentially enhanced in any given cardiac cell by conditions which elevate intracellular calcium. Such conditions include digitalis intoxication, high Cao, low Nao, low or high Ko, cooling, or rapid stimulation. Several lines of evidence suggest that the subcellular mechanism involves oscillatory variations in myoplasmic calcium, probably due to cycles of Ca uptake and release by the sarcoplasmic reticulum. The detailed nature of the Cai oscillator and its interaction with the surface membrane await further investigation.

Sign in / Sign up

Export Citation Format

Share Document