Author + information
- ↵*Address for reprints: Harry A. Fozzard, MD, Box 249, 5841 South Maryland Avenue, Chicago, Illinois 60637.
It has long been known that cardiac glycosides can inhibit the membrane sodium-potassium (Na+-K+) pump, raising intracellular Na+. However, at clinical concentrations of cardiac glycosides, a change in intracellular Na+that correlates with a change in cardiac contraction has been very difficult to demonstrate. The recent use of Na+-sensitive microelectrodes in the experimental laboratory has made intracellular Na+measurements possible. A doubling of contraction strength in vitro is associated with a change of only approximately 1 mMintracellular Na+. Another membrane transport system, the Na+-Ca2+exchange system, exchanges extracellular Na+ for intracellular Ca2+. If this system is responsible for regulating intracellular Ca2+, then it would be very sensitive to the transmembrane Na+ concentration gradient. This influence of intracellular Na+ on Na+-Ca2+exchange is thought to be the cellular basis of the positive inotropic action of digitalis. However, a number of issues remain unresolved, such as the extent of Na+-K+pump inhibition by the level of cardiac glycoside achieved clinically.
- American College of Cardiology Foundation