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

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 I_Ca.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 I_Ca.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.