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Effects of human recombinant interleukin-1 on electrical properties of guinea pig ventricular cells
1Department of Internal Medicine (Cardiology), University of Nebraska College of Medicine, Omaha 68189-4575.
Insights
Interleukin-1 beta (IL-1) alters cardiac cell electrical properties by affecting calcium channels. These effects involve lipid second messengers from cyclo-oxygenase and lipoxygenase pathways.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Inflammation and Immunity
Background:
- Cytokines, such as interleukin-1 beta (IL-1), are key mediators in inflammatory processes.
- The specific impact of IL-1 on the electrical properties of cardiac cells remains incompletely understood.
Purpose of the Study:
- To investigate the effects of IL-1 on the electrical characteristics of ventricular heart cells.
- To elucidate the underlying ionic mechanisms and signaling pathways involved in IL-1's cardiac effects.
Main Methods:
- Electrophysiological recordings of transmembrane potentials in isolated guinea pig papillary muscles.
- Patch-clamp analysis of L-type calcium current (ICa) in dissociated ventricular myocytes.
- Pharmacological assessment using cyclo-oxygenase and lipoxygenase pathway inhibitors.
Main Results:
- IL-1 significantly prolonged action potential duration and effective refractory period in papillary muscles.
- These prolongations were abolished by cyclo-oxygenase and lipoxygenase inhibitors, as well as a leukotriene receptor blocker.
- IL-1 increased L-type calcium current density in isolated ventricular myocytes.
Conclusions:
- IL-1 modulates cardiac cell electrical activity through lipid second messengers produced by both cyclo-oxygenase and lipoxygenase pathways.
- The observed electrophysiological changes are, at least partly, mediated by alterations in calcium channel conductance.
Objective:
To determine whether cytokines alter the electrical properties of heart cells, the effects of human recombinant interleukin-1 beta (IL-1) were examined in excised tissues and dissociated myocytes from guinea pig ventricles.
Methods:
In a first series of experiments, transmembrane potentials were recorded from isolated papillary muscles superfused with 1 ng.ml-1 IL-1 in the absence and presence of blockers of arachidonic acid metabolism. Secondly, to examine the ionic mechanisms underlying the response to IL-1, ventricular myocytes were dissociated from collagenase perfused hearts and studied using the whole cell configuration of the patch clamp technique under conditions designed to isolate the L-type Ca2+ current (ICa).
Results:
In excised papillary muscles, IL-1 significantly prolonged action potential duration (measured at 90% repolarisation) by 24.2(SEM 2.2) ms and effective refractory period by 22.9(2.3) ms (both p < 0.001; n = 44). Other measured variables were not affected. Treatment of muscles with cyclo-oxygenase inhibitors, indomethacin (1 x 10(-5) M) or acetyl salicylic acid (2 x 10(-4) M), abolished the prolongation of action potential duration elicited by IL-1. However, the effects of IL-1 were also blocked by the lipoxygenase inhibitor nordihydroguaiaretic acid (2 x 10(-5) M) or by treating tissues with the leukotriene receptor blocker, ICI198615 (1 x 10(-8) M). In isolated myocytes, 1 ng.ml-1 IL-1 increased ICa density in 44 of 78 cells by 33.6(7.5)% [11.7(0.6) v 14.6(0.7) pA.pF-1; p < 0.001] during voltage steps from -40 to 0 mV.
Conclusions:
IL-1 modifies electrical properties of cardiac cells via lipid second messengers generated by cyclo-oxygenase and lipoxygenase pathways. Voltage clamp analyses suggest that these effects are mediated, at least in part, by changes in the conductance of calcium channels.
