The effect of Na+‐Ca2+ exchange on the recovery from Ca2+ dependent inactivation of L‐type Ca2+ channel in cardiomyocytes in pulmonary vein

Abstract

Ca2+ dependent inactivation (CDI) of L‐type Ca2+ channel (CaL) is well known phenomena and Ca2+ release from SR greatly affected CaL kinetics, which was known as the release dependent inactivation (RDI). We would like to see whether L‐type Ca2+ kinetics were changed by Na+‐Ca2+ exchange (NCX) which would control the subsarcolemmal Ca2+. We used the isolated cardiomyocytes in main pulmonary vein of rabbit. RDI was induced by applying 2.5 msec prepulse from ‐40 mV to 10 mV and then the same amplitude of 50 msec test pulse was applied with various intervals. In the presence of 0.1 mM EGTA in the pipette solution, the inactivation tau (itau) was increased and the peak current amplitude (PCA) was decreased. As the interval was increased, itau and PCA were progressively returned to control ICaL. In the absence of bath Na+, the initial change was much larger and the recovery process was prolonged. In the presence of BAPTA 10 mM in the pipette solution, these phenomena were disappeared. Ryanodine or thapsigargin also attenuate these phenomena. In conclusion, NCX is an important regulator for the recovery of CaL from CDI by controlling subsarcolemmal Ca2+. (supported by NRF, 2009‐0076234)