scholarly journals The electrogenic sodium pump in guinea-pig ventricular muscle: inhibition of pump current by cardiac glycosides

1982 ◽  
Vol 330 (1) ◽  
pp. 243-264 ◽  
Author(s):  
Jürgen Daut ◽  
Reinhardt Rüdel
Keyword(s):  
Guinea Pig ◽  
Cardiac Glycosides ◽  
Sodium Pump ◽  
Pump Current ◽  
Ventricular Muscle ◽  
Electrogenic Sodium Pump ◽  
Muscle Inhibition

Sodium-Potassium Movement and the Regulation of Cardiac Muscle Activity

1982 ◽  
Vol 37 (7-8) ◽  
pp. 679-681
Author(s):  
Jürgen Daut ◽  
Reinhardt Rüdel
Keyword(s):  
Guinea Pig ◽  
Cardiac Muscle ◽  
Muscle Activity ◽  
Cardiac Glycoside ◽  
Sodium Pump ◽  
Ventricular Muscle ◽  
Sodium Potassium ◽  
Sodium Activity ◽  
Electrogenic Sodium Pump ◽  
Fast Acting

Abstract The changes in intracellular sodium activity and contractility produced by short-lasting application of a fast-acting cardiac glycoside were measured in guinea-pig ventricular muscle. It was found that under certain conditions the change in twitch tension paralleled the change in sodium activity. It is suggested that the electrogenic sodium pump may be involved in the regulation of both the mechanical and the electrical activity of cardiac muscle.

Sodium-pump potentials and currents in guinea-pig ventricular muscles and myocytes

1999 ◽  
Vol 77 (5) ◽  
pp. 339-349 ◽  
Author(s):  
Yuji Kasamaki ◽  
An Chi Guo ◽  
Lesya M Shuba ◽  
Toshitsugu Ogura ◽  
Terence F McDonald
Keyword(s):  
Guinea Pig ◽  
Voltage Clamp ◽  
Cardiac Glycosides ◽  
Sodium Pump ◽  
Pump Current ◽  
Papillary Muscles ◽  
Maximal Concentration ◽  
Sodium Pump Current ◽  
Reproducible Manner

When guinea-pig papillary muscles were depolarized to ca. -30 mV by superfusion with K+-free Tyrode's solution supplemented with Ba2+, Ni2+, and D600, addition of Cs+ transiently hyperpolarized the membrane in a reproducible manner. The size of the hyperpolarization (pump potential) depended on the duration of the preceding K+-free exposure; peak amplitudes (Epmax) elicited by 10 mM Cs+ after 5-, 10-, and 15-min K+-free exposures were 12.9, 17.7, and 23.2 mV, respectively. Pump potentials were unaffected by external Cl- but suppressed by cardiac glycosides, hyperosmotic conditions, and low-Na+ solution. Using Epmax as an indicator of Na+ pump activation, the half-maximal concentration for activation by Cs+ was 12-16.3 mM. At 6 mM, Cs+ was three times less potent than Rb+ or K+ and five times more potent than Li+. From these findings, and correlative voltage-clamp data from myocytes, we calculate that (i) a pump current of 7.8 nA/cm2 generates an Epmax of 1 mV and (ii) resting pump current in normally polarized muscle (~0.16 µA/cm2) is five times smaller than previously estimated.Key words: sodium pump, cesium, rubidium, sodium pump current.

The Effects of Sodium-Transport Inhibitors and Cooling on Membrane Potentials in Cockroach Central Nervous Connectives

1974 ◽  
Vol 61 (1) ◽  
pp. 203-218
Author(s):  
Y. PICHON ◽  
J. E. TREHERNE
Keyword(s):  
Sodium Transport ◽  
Cardiac Glycosides ◽  
Sodium Pump ◽  
Ethacrynic Acid ◽  
Membrane Potentials ◽  
Appreciable Effect ◽  
Electrogenic Sodium Pump ◽  
Sucrose Gap ◽  
Transport Inhibitors ◽  
Sodium Regulation

1. Cooling caused axonal depolarization in desheathed and urea-treated connectives, but induced hyperpolarizing responses (measured with micro-electrodes and with the sucrose-gap) in intact preparations. Hyperpolarizing responses were also recorded with extracellularly-located microelectrodes in intact connectives. 2. Strophanthidin (0.2 mM/l) caused axonal depolarization in desheathed preparations, ethacrynic acid being without appreciable effect. Ethacrynic acid (0.2 mM/1) induced apparent hyperpolarizations in intact connectives and abolished or reduced the effects of cooling. 3. It is concluded that the axonal sodium pump is pharmacologically separable from that associated with the perineurial and/or the glial membranes: the former being inhibited by cardiac glycosides, the latter by ethacrynic acid. 4. The results are discussed in relation to extra-axonal sodium regulation and the possible involvement of an electrogenic sodium pump associated with the perineurial or glial membranes.

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