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Updated: Aug 14, 2026
Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
[Effect of interleukin-2 on intracellular calcium transients in rat ventricular myocytes]
1Department of Physiology, Zhejiang University School of Medicine, Hangzhou 310031, China. xiaqiang@cmm.zju.edu.cn
Insights
Interleukin-2 (IL-2) depresses intracellular calcium transients in heart cells via kappa opioid receptors. This effect involves Gi-protein and phospholipase C, not tyrosine kinase, impacting cardiac function.
Area of Science:
- Cardiology
- Molecular Pharmacology
- Cell Physiology
Context:
- Interleukin-2 (IL-2) plays a role in immune responses but its effects on cardiac function are not fully understood.
- Intracellular calcium (Ca2+) transients are critical for cardiomyocyte contraction and overall heart function.
- Understanding signaling pathways involved in IL-2's cardiac effects is crucial for potential therapeutic interventions.
Purpose:
- To investigate the impact of IL-2 on intracellular calcium handling in ventricular myocytes.
- To elucidate the specific signaling pathways, including opioid receptors and protein interactions, mediating IL-2's effects on cardiac Ca2+ transients.
Summary:
- Interleukin-2 (IL-2) was found to dose-dependently reduce electrically induced Ca2+ transients in isolated ventricular myocytes.
- The inhibitory effect of IL-2 was abolished by kappa opioid receptor antagonists (naloxone, nor-BNI) and pertussis toxin (PTX)-sensitive Gi-protein and phospholipase C (PLC) inhibition.
- IL-2's action was independent of the caffeine-releasable Ca2+ pool and did not involve delta opioid receptors or tyrosine kinase pathways.
Impact:
- Reveals a novel mechanism for IL-2's influence on cardiac electrophysiology via the kappa opioid receptor pathway.
- Highlights the involvement of Gi-protein and PLC in mediating IL-2's cardiac depressant effects.
- Provides insights into the molecular targets for modulating IL-2's cardiovascular actions.
Abstract:
In the present study, we investigated the effect of interleukin-2 (IL-2) on the intracellular calcium in enzymatically isolated ventricular myocytes with the use of the spectrofluorometric techniques. It was shown that IL-2 (2.5 200 U/ml) depressed electrically induced Ca(2+) (i) transients of ventricular myocytes in a dose dependent manner. IL-2 (200 U/ml) did not alter the caffeine releasable pool of Ca(2+). Pretreatment with the non selective opioid antagonist naloxone (10(-8)mol/L) or a specific kappa opioid antagonist nor binaltorphimine (nor-BNI, 10(-8) mol/L) abolished the inhibitory effect of IL-2 (200 U/ml) on the Ca(2+) (i) transients of cardiomyocytes, whereas the specific delta opioid antagonist naltrindole (10(-6) mol/L) did not abolish the inhibitory effect. The effect of IL-2 (200 U/ml) was also abolished after pretreatment with pertussis toxin (PTX, 5 mg/L) as well as phospholipase C (PLC) inhibitor U73122 (5 10(-6) mol/L), but not by tyrosine kinase inhibitor genistein (10(-4) mol/L). It is concluded that the depressant effect of IL-2 on the Ca(2+) (i) transients of isolated ventricular myocytes is mainly mediated by cardiac kappa opioid receptor pathway including a PTX sensitive Gi-protein and PLC, but not by tyrosine kinase.
