The intracellular sodium activity of cardiac Purkinje fibres during inhibition and re-activation of the Na-K pump. 1978

J W Deitmer, and D Ellis

1. The intracellular Na activity, aiNa, of sheep heart Purkinje fibres was continuously monitored using Na+-sensitive glass micro-electrodes. The effects of removal and restoration of external K, and of application and removal of various cardioactive steroids, were investigated. 2. The aiNa increased in K-free solutions and rapidly recovered on addition of external K. The rate of this recovery depended on both the external K concentration, [K]o, and the aiNa. The rate of aiNa recovery was found to be half maximally activated at a [K]o of about 10 mM. If corrections are applied to allow for changes in the net passive Na influx at various [K]o, then this value is increased to approximately 12.5 mM. 3. At a given [K]o, there appeared to be a linear relationship between the rate of aiNa recovery and the level to which aiNa had increased in K-free solution (over the range of aiNa from 7.5 to 31 mM). 4. Addition of the cardioactive steroids strophanthidin, acetylstrophanthidin, actodigin (AY 22,241) or dihydro-ouabain produced rapid changes of aiNa. At low concentrations, these compounds sometimes produced a small decrease in aiNa, while at concentrations above 10(-7) M they produced a dose-dependent increase. 5. The effects on aiNa of both low and high concentrations of all these cardioactive steroids were readily reversible within 120 min. The time course of the aiNa recovery mainly depended on the concentration of the cardioactive steroid applied, and on the level to which aiNa had increased. 6. Upon addition of a cardioactive steroid (above 10(-7) M, aiNa at first increased almost linearly with time. The rates of such an increase were measured during this period at various cardioactive steroid concentrations and used to produce dose-response curves. The concentrations that produced a half-maximum rate of aiNa increase were near to 10(-6) M for strophanthidin and acetylstrophanthidin, but near to 10(-5) M for actodigin and dihydro-ouabain. 7. The mean maximum rate of aiNa increase produced by the addition of a high cardioactive steroid concentration was 0.49 +/- 0.17 mM/min (+/-S.D., n = 21). This would indicate a net passive Na influx into the cells of approximately 2.8 p-mole/cm2sec. 8. This maximum rate of aiNa increase could be achieved by the addition of 10(-5) M-strophanthidin or acetylstrophanthidin, but 10(-4) to 10(-3) M-actodigin or dihydro-ouabain was required to produce a similar rate of increase. 9. The addition of these high cardioactive steroid concentrations produced an initially rapid increase of aiNa. After 15-30 min this aiNa increase slowed considerably. The aiNa appeared to reach a 'plateau' within 2-4 hr at levels much below those predicted for a Na electrochemical equilibrium across the cell membrane.

UI MeSH Term Description Entries
D007424 Intracellular Fluid The fluid inside CELLS. Fluid, Intracellular,Fluids, Intracellular,Intracellular Fluids
D007700 Kinetics The rate dynamics in chemical or physical systems.
D010042 Ouabain A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE. Acocantherin,G-Strophanthin,Acolongifloroside K,G Strophanthin
D011188 Potassium An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
D011690 Purkinje Fibers Modified cardiac muscle fibers composing the terminal portion of the heart conduction system. Purkinje Fiber,Fiber, Purkinje,Fibers, Purkinje
D002298 Cardenolides C(23)-steroids with methyl groups at C-10 and C-13 and a five-membered lactone at C-17. They are aglycone constituents of CARDIAC GLYCOSIDES and must have at least one double bond in the molecule. The class includes cardadienolides and cardatrienolides. Members include DIGITOXIN and DIGOXIN and their derivatives and the STROPHANTHINS. Cardenolide
D002301 Cardiac Glycosides Cyclopentanophenanthrenes with a 5- or 6-membered lactone ring attached at the 17-position and SUGARS attached at the 3-position. Plants they come from have long been used in congestive heart failure. They increase the force of cardiac contraction without significantly affecting other parameters, but are very toxic at larger doses. Their mechanism of action usually involves inhibition of the NA(+)-K(+)-EXCHANGING ATPASE and they are often used in cell biological studies for that purpose. Cardiac Glycoside,Cardiotonic Steroid,Cardiotonic Steroids,Glycoside, Cardiac,Glycosides, Cardiac,Steroid, Cardiotonic,Steroids, Cardiotonic
D004071 Digitalis Glycosides Glycosides from plants of the genus DIGITALIS. Some of these are useful as cardiotonic and anti-arrhythmia agents. Included also are semi-synthetic derivatives of the naturally occurring glycosides. The term has sometimes been used more broadly to include all CARDIAC GLYCOSIDES, but here is restricted to those related to Digitalis. Glycosides, Digitalis
D004305 Dose-Response Relationship, Drug The relationship between the dose of an administered drug and the response of the organism to the drug. Dose Response Relationship, Drug,Dose-Response Relationships, Drug,Drug Dose-Response Relationship,Drug Dose-Response Relationships,Relationship, Drug Dose-Response,Relationships, Drug Dose-Response
D006329 Heart Conduction System An impulse-conducting system composed of modified cardiac muscle, having the power of spontaneous rhythmicity and conduction more highly developed than the rest of the heart. Conduction System, Heart,Conduction Systems, Heart,Heart Conduction Systems,System, Heart Conduction,Systems, Heart Conduction

Related Publications

J W Deitmer, and D Ellis
January 1992, Journal of molecular and cellular cardiology,
J W Deitmer, and D Ellis
March 1988, The Journal of general physiology,
J W Deitmer, and D Ellis
June 1980, The Journal of physiology,
J W Deitmer, and D Ellis
June 1980, The Journal of physiology,
J W Deitmer, and D Ellis
September 1982, Pflugers Archiv : European journal of physiology,
J W Deitmer, and D Ellis
May 1989, Pflugers Archiv : European journal of physiology,
J W Deitmer, and D Ellis
May 1983, Pflugers Archiv : European journal of physiology,
Copied contents to your clipboard!