Contributions of Ca2+-influx via the L-type Ca2+-current and Ca2+-release from the sarcoplasmic reticulum to [Ca2+]i-transients in human myocytes

Experiments were performed to determine the relative contributions of direct Ca2+-entry through the L-type Ca2+-current and of Ca2+-release from the sarcoplasmic reticulum (s.r.) to the intracellular [Ca2+]i-transient in isolated human atrial and ventricular myocytes from patients with severe heart failure and from non-failing controls. Cells were isolated from explanted hearts of patients undergoing transplantation because of severe heart failure due to dilated or ischemic cardiomyopathy or from donor hearts which could not be transplanted for technical reasons. Ca2+-current densities were −2.1±0.6 pA/pF in atrial cells, −4.8±0.5 pA/pF in cells from patients with heart failure and −3.2±0.5 pA/pF in non-failing controls. [Ca2+]i-transients were significantly smaller in heart failure (370±33 nM) compared to ventricular cells from non-failing hearts (760±69 nM, p<0.05). Atrial myocytes had average [Ca2+]i-transients of 505±38 nM. After incubation in ryanodine the average [Ca2+]i-transients were not significantly different between different cell types.