Study of the remodeling of L-type calcium channel in ventricular myocytes with chronic heart failure

Objective To explore the remodeling of L-type calcium channel in ventricular myocytes with chronic heart failure(CHF).Methods Thirty rats were randomly divided into CHF group and Sham group.CHF rat model of abdominal aortic banding was established.Whole cell patch clamp technique was used to record L-type calcium ion current(ICa,L),describe the steady-state activation curve,steady-state inactivation curve,recovery curve after deactivation of ICa,L.The expression of L-type calcium channel ɑ1c subunits were also detected by immunohistochemistry.Results The left ventricular end-systolic pressure,the maximum increase rate of left ventricular pressure,the maximum decrease rate of left ventricular pressure and LVEF of CHF group were significant lower than those of sham group(P0.01),the left ventricular end-diastolic pressure of CHF group was significant higher than that of sham group(P0.01).The current density amplitude of ICa,L in CHF group was decreased significantly than that of sham group [-(5.03±0.51) pA/pF vs-(8.14± 0.54) pA/pF,P0.01]) and I-V curve was evaluated.Compared with sham group,the steady-state activation curve of CHF group was shift to right.The V1/2,act amplitude of CHF group was significant higher than that of sham group [-(3.9±0.11) mV vs-(2.8±0.10)mV,P0.01].The κact of CHF group was significant lower than that of sham group(6.1±1.3 mV vs 7.7±1.2 mV,P0.01). There were no significant difference between the two group in steady-state inactivation curve,V1/2,inact and κinact.Compared with sham group,the recovery curve after deactivation of CHF group was shift to right.The τ value of CHF group was significant bigger than that of sham group(39.8±3.3 ms vs 26.3±2.9 ms,P0.05).Compared with sham group,the expression of L-type channel current ɑ1c subunit was lower in CHF group(P0.01).Conclusions During CHF,the remodeling characteristic of L-type channel causes the ICa,L current density decrease.These may play an important role in the development of ventricular tachycardia in CHF.