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Updated: Jul 16, 2026
Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Na+/Ca2+ exchange currents and SR Ca2+ contents in postinfarction myocytes
X Q Zhang1, D L Tillotson, R L Moore
1Department of Medicine, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
Abstract:
Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had lower peak cytosolic free Ca2+ concentration ([Ca2+]i) and reduced maximal extent of cell shortening during contraction, but Ca2+ entry via L-type Ca2+ channels was normal. In the current study using whole cell patch-clamp technique, reverse Na+/Ca2+ exchange current (INa/Ca; 3 Na+ out:1 Ca2+ in) was measured in myocytes in which Na+, K+, and Ca2+ currents were blocked or minimized. Steady-state outward currents measured under these conditions increased with depolarization or with elevation of extracellular Ca2+ concentration ([Ca2+]o) from 1.8 to 5.0 mM, but were inhibited by 5 mM Ni2+ or by reduction of [Ca2+]i to near zero. In addition, reduction of cytosolic free Na+ concentration or of [Ca2+]i also decreased the amplitude of the outward current. These characteristics indicate the outward current was INa/Ca operating in reverse mode. Reverse INa/Ca was significantly lower in MI myocytes, especially at more positive voltages. In addition, sarcoplasmic reticulum (SR)-releasable Ca2+ content as estimated by integrating forward INa/Ca during caffeine-induced SR Ca2+ release was also significantly lower in MI myocytes. Depressed Na+/Ca2+ exchange activity may contribute to abnormal [Ca2+]i dynamics in MI myocytes.
Insights
Myocardial infarction (MI) in rats impairs cardiac function by reducing reverse sodium-calcium exchange (INa/Ca) and sarcoplasmic reticulum calcium release. This dysfunction contributes to abnormal intracellular calcium handling in heart cells post-MI.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Cardiac Pathophysiology
Background:
- Myocytes from rats post-myocardial infarction (MI) exhibit reduced peak cytosolic calcium and impaired contraction.
- Calcium entry via L-type calcium channels remains normal in these MI myocytes.
Purpose of the Study:
- To investigate the role of reverse sodium-calcium exchange current (INa/Ca) in myocytes following myocardial infarction (MI).
- To assess sarcoplasmic reticulum calcium content in MI myocytes.
Main Methods:
- Whole-cell patch-clamp technique was employed to measure reverse Na+/Ca2+ exchange current (INa/Ca).
- Ionic currents were minimized to isolate and quantify INa/Ca under varying conditions.
- Sarcoplasmic reticulum (SR) releasable calcium was estimated via caffeine-induced SR calcium release.
Main Results:
- Reverse INa/Ca was significantly lower in MI myocytes compared to controls, particularly at positive voltages.
- Outward currents exhibiting characteristics of reverse INa/Ca were dependent on extracellular calcium and inhibited by nickel.
- SR-releasable calcium content was also significantly reduced in MI myocytes.
Conclusions:
- Depressed reverse sodium-calcium exchange activity is a key finding in myocytes after myocardial infarction.
- Reduced INa/Ca and impaired SR calcium release likely contribute to abnormal intracellular calcium dynamics in MI.
- These ionic dysregulations may underlie the observed contractile dysfunction in post-MI hearts.
