Modulation of L-Type Calcium Current by Calcium-Dependent Mechanism in Trout Ventricular Myocytes

Abstract

In cardiac myocytes, Ca has a dual role upon of L-type calcium current (ICa) by either inactivating it (calcium-dependent inactivation, CDI) or facilitating it (calcium-dependent facilitation, CDF). In fish cardiac myocytes, it is unclear whether both Ca modulations exist. This study addresses this point. Trout ventricular myocytes were enzymatically isolated. ICa was recorded using whole cell patch clamp with Na- and K-free solutions to avoid contaminating currents. With a low concentration of a slow Ca buffer (EGTA 2mM) in the pipette solution, ICa inactivated slowly (compared to mammalian cardiac myocytes): the time to reach 37% of peak current (T37) was 26.2± 2.4 ms (mean±SEM, n=14). CDF was absent in all cells studied. When a fast Ca buffer (BAPTA 10 mM) was present in the pipette solution, ICa decay was similar to the decay in the presence of EGTA (T37: 25.4±1.5 ms, NS, t-test, n=9) and CDF was absent (n=9). We quantified the relative contribution of CDI and sarcoplasmic reticulum (SR) CDI according to our published method, and estimated that CDI represents ∼39% of total ICa inactivation, and that SR Ca release causes ∼12% of CDI. We conclude that in fish myocytes CDI play a role in ICa modulation but CDF is absent.Supported by the Welcome Trust.