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 (I(Ca)) 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 I(Ca) 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.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||5 48-5|
|Publication status||Published - 12 Dec 2000|
- Excitation-contraction coupling
- L-type calcium current