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10.07.2018 | Ausgabe 1/2019

Cardiovascular Toxicology 1/2019

Long-Term IL-2 Incubation-Induced L-type Calcium Channels Activation in Rat Ventricle Cardiomyocytes

Cardiovascular Toxicology > Ausgabe 1/2019
Tatiana Filatova, Vadim Mitrokhin, Olga Kamkina, Irina Lovchikova, Mitko Mladenov, Andre Kamkin
Wichtige Hinweise
Handling Editor: Y. James Kang.


The following study examined the impact of IL-2 on Ca2+ channel activity in the event of several hours’ incubation in IL-2. The right ventricle free wall for action potential measurements was isolated and perfused with Tyrode solution. The whole-cell voltage clamp experiments were performed on enzymatically isolated single cardiomyocytes. The whole-cell voltage clamp recording of Ca2+ currents was performed using the Cs+-based pipette and bath solutions. The protocol with depolarizing prepulse (− 40 mV) was used to inactivate both Na+ current and Ca2+T-type current. The L-type Ca2+ current was elicited by a series of 250 ms depolarizing square pulses with 10 mV increments. At the 15th minute of continuous recording, the peak density at 0 mV was − 3.036 ± 0.3015 pA/pF under IL-2 and − 3.008 ± 0.3452 pA/pF in control conditions. The IL-2 in moderate concentration (1 ng/mL) has no acute effects on ICa.L in rat ventricular cells. In contrast, to the lack of acute effects, the long-term incubation with IL-2 (2 h or more) produced a prominent enhancement of Ca2+L-type current. In rat, ventricular myocardium IL-2 (1 ng/mL) produced a very gradual prolongation of subendocardial APs which reached a maximal extent after 3–4 h of treatment. The patch clamp study shows an IL-2-induced ICa.L current activation, while the action potential studies on multicellular ventricular preparations suggest an IL-2-induced L-type Ca2+ channel participation in the development of AP.

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