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Department of Physiology, Cell Biology and Immunology, Faculty of Science, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain
We have used the whole cell configuration of the
patch-clamp technique to measure sarcolemmal Ca2+ transport
by the Na+/Ca2+ exchanger (NCX) and its
contribution to the activation and relaxation of contraction in trout
atrial myocytes. In contrast to mammals, cell shortening continued,
increasing at membrane potentials above 0 mV in trout atrial myocytes.
Furthermore, 5 µM nifedipine abolished L-type Ca2+
current (ICa) but only reduced cell shortening
and the Ca2+ carried by the tail current to 66 ± 5 and 67 ± 6% of the control value. Lowering of the pipette
Na+ concentration from 16 to 10 or 0 mM reduced
Ca2+ extrusion from the cell from 2.5 ± 0.2 to
1.0 ± 0.2 and 0.5 ± 0.06 amol/pF. With 20 µM exchanger
inhibitory peptide (XIP) in the patch pipette Ca2+
extrusion 20 min after patch break was 39 ± 8% of its initial value. With 16, 10, and 0 mM Na+ in the pipette, the
sarcoplasmic reticulum (SR) Ca2+ content was 47 ± 4, 29 ± 6, and 10 ± 3 amol/pF, respectively. Removal of
Na+ from or inclusion of 20 µM XIP in the pipette
gradually eliminated the SR Ca2+ content. Whereas
ICa was the same at 
10 or +10 mV,
Ca2+ extrusion from the cell and the SR Ca2+
content at 10 mV were 65 ± 7 and 80 ± 4% of that at +10
mV. The relative amount of Ca2+ extruded by the NCX (about
55%) and taken up by the SR (about 45%) was, however, similar with
depolarizations to 10 and +10 mV. We conclude that modulation of the
NCX activity critically determines Ca2+ entry and cell
shortening in trout atrial myocytes. This is due to both an alteration
of the transsarcolemmal Ca2+ transport and a modulation of
the SR Ca2+ content.
caffeine; L-type calcium current; cardiac; excitation-contraction coupling
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