Membrane current and contraction in frog atrial fibres

Abstract

1. Membrane current and mechanical activity were recorded from short segments of frog atrial muscle strips using a double sucrose gap voltage clamp arrangement. Experiments were performed at 4–7° C. Two types of contraction were observed dependent upon the duration of the clamp. 2. Short-lasting depolarizations caused a flow of Ca inward current, I_Ca, and development of a phasic contraction. Time to peak tension approximated 400 msec. Both I_Ca and contraction, as functions of membrane potential, had a threshold of about — 40 mV and were maximal at inside positive potentials in normal Ringer fluid. Peak tension decreased at strong depolarizations. 3. The minimum time of depolarization required for initiation of a phasic contraction was 40–70 msec. The time necessary for full activation of contraction was 200–300 msec and comparable to the period of time covered by the flow of I_Ca. 4. There was no marked change in peak tension upon repetitive depolarization to the same membrane potential. 5. Restoration of (phasic) contractility after a preceding contraction was strongly dependent on the level of membrane potential between conditioning and test pulse. Restoration was half complete at potentials around — 45 mV. 6. Long-lasting depolarizations generated tonic (sustained) contractions superimposed on the phasic (transient) ones. Threshold potential for initiation of tonic contractions was usually positive to the threshold of phasic contractions. The time taken to attain the final level of tension ranged between 0·7 and 3 sec. Plateau tension, as a function of membrane potential, increased with increasing depolarization and reached a flat maximum at about + 50 mV in normal Ringer fluid. 7. At membrane potentials near zero level, plateau tension developed by the tonic mechanism was about twice peak tension due to phasic contraction. 8. Removal of Ca ions from the external medium resulted in an almost complete abolition of phasic contraction within 1–2 min and a gradual decrease of tonic contraction during the first 10 min. Application of a ‘Ca inhibitor’ to normal Ringer fluid caused a strong reduction of both I_Ca and phasic contraction without affecting tonic contractions. 9. It is concluded that phasic contractions are directly activated by the flow of I_Ca. Generation of tonic contractions may be attributed to a Ca transfer mechanism different from I_Ca or a release of Ca from intracellular stores.