Voltage-tension relations in single frog atrial cardiac cells.

Abstract

Voltage-clamp experiments were performed on isolated single frog (Rana catesbeiana or Rana pipiens) atrial cells to determine the voltage-contraction relations of the single cardiac cell. The contractile responses of the single cell associated with long duration (3 second) depolarizing steps consisted of a rise to peak (phasic) followed by a decay to a sustained contraction (tonic). These phasic-tonic type contractile responses could be obtained under conditions where membrane potential was well controlled along the entire length of the cell. Thus, the data obtained on the single cell indicate that the phasic-tonic contractile response is the characteristic contractile response of frog atrial tissue. The voltage dependence of the extent of relaxation to the tonic component following the peak of the contraction was affected dramatically by the intracellular sodium concentration. This result indicates that both the relaxation following peak contraction as well as the tonic contraction are related to calcium control via the sodium-calcium exchanger. The data also indicate that calcium entry via the inward calcium current is required for the contractile response to have a phasic component. These data indicate that calcium entry via the inward calcium current followed by the sodium-calcium exchanger first reducing and then maintaining the intracellular calcium level produces the characteristic phasic-tonic contractile response.

"Creep currents" in single frog atrial cells may be generated by electrogenic Na/Ca exchange.

“…If aCa is higher than estimated or if a Na is lower than estimated, then the current-voltage relationship for the exchanger may be displaced in the positive direction on the voltage axis under normal conditions . The recent finding that the tonic tension-voltage relationship in single frog atrial cells under normal conditions may occur at significantly more depolarized potentials than indicated by previous determinations in multicellular preparations may be consistent with this (Tarr et al, 1985). We might speculate that under these conditions, inward creep currents may contribute more significantly to the electrical activity of the cell during membrane depolarizations up to 0 mV or even more positive .…”

Studies of the sodium‐calcium exchanger in bull‐frog atrial myocytes.

“…These results suggested that tonic tension was being generated by the Na+-Ca2+ exchanger, and that this process must be electrogenic and voltage dependent. These results have recently been confirmed in single frog atrial cells by Tarr, Trank & Goertz (1986). Mentrard, Vassort & Fischmeister (1984) reported identification of a current which: (i) was modulated by the Na+ gradient, (ii) was inhibited by La3+, and (iii) had approximately the voltage dependence predicted by the Mullins' (1979Mullins' ( , 1981 model of electrogenic Na+-Ca2a exchange.…”

“…Furthermore, Potreau & Raymond (1985) have recently shown that tonic tension in frog atrial trabeculae is inhibited when Ba2+ is substituted for Ca2+. This is a very relevant finding, since tonic tension in frog heart is hypothesized to be generated by Ca2+ influx produced by the Na+-Ca2+ exchanger operating in 'reverse mode' (Horackova & Vassort, 1979;Chapman, 1979Chapman, , 1983Tarr et al 1986). These results in combination with our data suggest that the slow tails may be generated by the Na+-Ca2+ exchanger operating in 'forward mode' (i.e.…”

Modulation of contraction by intracellular Na+ via Na(+)‐Ca2+ exchange in single shark (Squalus acanthias) ventricular myocytes.

“…Recent evidence indicates that the Na+-Ca2+ exchange is electrogenic and may contribute to Ca2+ influx into as well as Ca2+ extrusion from the cell, depending on membrane potential and transmembrane ion gradients for Na+ and Ca2+ (Mullins, 1979;Mechmann & Pott, 1986). The Na+-Ca2+ exchange mechanism has been suggested to mediate both Ca2" influx responsible for the tonic component of developed tension in myocardium as well as extrusion of Ca2+ and the relaxation of contraction (Horackova & Vassort, 1979;Horackova, 1984Horackova, , 1985Chapman & Rodrigo, 1985;Tarr, Trank & Goertz, 1986;Bridge, Spitzer & Ershler, 1988;Horackova, Beresewicz & Isenberg, 1988). Variations of [Na+]i, sufficient to alter significantly the trans-sarcolemmal Na+ gradient may thus be critical for Ca2+ handling of the cell.…”