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

Basic Research in Cardiology, ISSN: 1435-1803, Vol: 92, Issue: 1 SUPPL., Page: 105-110
1997
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Experiments were performed to determine the relative contributions of direct Ca-entry through the L-type Ca and of Ca -release from the sarcoplasmic reticulum (s.r.) to the intracellular [Ca]-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 trans- plantation because of severe heart failure due to dilated or ischemic cardiomyopathy or from donor hearts which could not be transplanted for technical reasons. Ca-current densities were -2.1 ± 0.6 pA/pF in atrial cells, -4.8 ± 0.5 pA/pFin cells from patients with heart failure and -3.2 ± 0.5 pA/pF in non-failing controls. [Ca ]-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 [Ca ]-transients of 505 ± 38 nM. After incubation in ryanodine the average [Ca]-transients were not significantly different between different cell types. The results indicate that the relative contribution of Ca released from the sarcoplasmic reticulum to the [Ca]-transient is significantly smaller in heart failure. The absolute contribution of the L-type Ca -current to the transient seemed to be comparable in all cell types investigated. As the [Ca]-transient in the presence of ryanodine was comparable in size in all cells, changes of the intracellular [Ca]-transient in heart failure are mainly due to alterations of s.r. function in these cells. © Steinkopff Verlag 1997.

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