Generation of twitch tension in frog atrial fibers by Na/Ca exchange.
Electrical and mechanical responses of frog atrial trabeculae were studied simultaneously using the double-sucrose gap method. Action potentials and twitch tension could be successively generated in fibers in which the slow inward calcium channel current was not observed. As a rule, this could be obtained in the course of a long experiment (3 to 4 hours). Peak tension was shown to increase monotonically with membrane potential in these preparations. In preparations with the slow inward current the total peak tension could be separated into two components. The first component (tonic) monotonically increased with the membrane potential and was probably related to Na/Ca exchange (Horackova 1984). The potential dependency of the second (phasic) component correlated with that of the slow inward calcium current. Only the tonic but not the phasic component could be observed in preparations without the presence of the slow inward calcium current. The tonic component prevailed when both the slow inward current and phasic tension were greatly reduced by nifedipine. Long experiments, long depolarizing clamp pulses, a metabolic inhibitor 2,4-dinitrophenol, inhibitors of Na/K pump ouabain and AR-L57, toxins promoting intracellular sodium accumulation (aconitine, scorpion toxin) were all shown to increase the tonic tension, but not the slow inward current; they induced a transition from biphasic tension-voltage curve into a monotonically increasing one. We concluded that these procedures and agents greatly stimulate Ca influx via Na/Ca exchange. These results show that Na/Ca exchange can function as a reserve system of Ca2+ used for contraction, thus supporting the heart function, especially under unfavourable metabolic conditions.
Filippov
A K
AK
Chemical Products Biological Testing Research Institute, Kupavna, Moscow, USSR.
Tertishnikova
S M
SM
Bouquet
T I
TI
Porotikov
V I
VI
Ilyin
V I
VI
D019297:2,4-Dinitrophenol; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D016275:Atrial Function; D002118:Calcium / Q000378:metabolism*; D004140:Dinitrophenols / Q000494:pharmacology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000187:drug effects; D009543:Nifedipine / Q000494:pharmacology; D011895:Rana ridibunda; D012964:Sodium / Q000378:metabolism*
D004140:Dinitrophenols; D007473:Ion Channels; D012964:Sodium; D009543:Nifedipine; D019297:2,4-Dinitrophenol; D002118:Calcium