P. Arlock et al., POTENTIATION OF THE CONTRACTION FOLLOWING A PROLONGED DEPOLARIZATION IN ISOLATED FERRET MYOCARDIUM, Acta Physiologica Scandinavica, 163(1), 1998, pp. 3-11
The contractile force was studied in ferret papillary muscles during v
oltage clamp depolarizations, using the single sucrose gap method. Pro
longation of a test depolarization within a train produced potentiatio
n of the following contraction. The effects of varied duration and mem
brane potential of the test depolarization upon the potentiated force
of the following beat were studied. We assumed that force of a beat wa
s an index of calcium entry on the previous depolarization. The relati
onship between the peak contractile force of the following potentiated
beat and the systolic membrane potential of the test depolarization r
evealed an equilibrium around -18 mV. This was manifest after 100 ms o
f no effect. Positive potentials caused potentiation of force of the f
ollowing beat; negative potentials caused suppression of force of the
following beat. Calcium entry, if carried by an electrogenic exchange
mechanism, would be revealed as a membrane current developing after 10
0 ms. Membrane current at these times was always outward. When the dur
ation of the test depolarization was prolonged, outward current prior
to repolarisation progressively increased. When the duration of the te
st depolarization was held constant, outward current was varied by var
iation in membrane potential. Force of the following beat was proporti
onal to the test clamp membrane potential. The potentiation of the con
traction following a prolonged depolarization was abolished by substit
uting 75% of the sodium in the perfusion medium with lithium. These re
sults are compatible with the hypothesis that potentiation of force fo
llowing a prolonged depolarization is derived from calcium entry into
myocardial cells by reversed sodium-calcium exchange.