Excitation—contraction coupling in frog ventricle: evidence from voltage clamp studies

Abstract

SUMMARY1. Membrane potential, tension and membrane current were simultaneously recorded from frog ventricular strips in a modified sucrose-gap which enabled control of membrane potential by voltage clamp.2. Shortening the frog ventricular action potential by repolarizing the membrane to the resting potential terminates contraction. 3. Depolarization to the level of the normal action potential plateau for longer than about 80-100 msec (up to 30 sec) produces and maintains tension for the duration of the depolarization.4. Depolarizations less than about 80 msec in duration generate no tension but can facilitate the tension response to subsequent depolarizations. The facilitating effect of a short depolarizing pulse persists for no longer than 0 5 sec.5. The mechanical threshold is about -50 mV; the relation between membrane potential and tension is fairly linear from about + 5 to + 80 mV.6. Variation of holding potential, below the mechanical threshold, has no effect on the tension-voltage relation. The absolute membrane potential rather than pulse amplitude determines the developed tension.7. Increasing external calcium increases the slope of the voltage-tension relation.8. Contraction of the frog ventricle is directly controlled by the electrical activity of the surface membrane.

The ionic dependence of the strength and spontaneous relaxation of the potassium contracture induced in the heart of the frog Rana pipiens

“…More recently, with the advent of the sucrose-gap technique several reports have described the relationship between the membrane potential and the tension developed by cardiac muscle. It is noticeable that two different types of relationship have been obtained; either a simple sigmoidal (Beeler & Reuter, 1970b;Morad & Orkand, 1971), or an N-shaped curve has been found (Ochi & Trautwien, 1971;Vassort & Rougier, 1972;Leoty et al 1971;Gibbons & Fozzard, 1971 a). In the present work, using a variation of the [K]o to alter the membrane potential, no N-shaped tension-depolarization curves have been found.…”

“…At least part of the ionic calcium that activates contraction in frog heart comes directly from the bathing medium when the membrane is depolarized. This calcium has been supposed to act as a trigger for further release of calcium from intracellular sites as well as contributing to activation of the contractile apparatus itself (Chapman & Tunstall, 1971;Chapman, 1971a), or it has been thought to be sufficient to activate contraction in its own right (Morad & Orkand, 1971). In either case, if when the membrane is depolarized the release of calcium ions into the sarcoplasm commences and continues throughout the period of depolarization, it will be the influx from the outside medium that will eventually contribute the major part of the activator calcium, because the intracellular stores will have a finite capacity.…”

Potassium currents in frog ventricular muscle: evidence from voltage clamp currents and extracellular K accumulation.

“…A tentative model for inward rectifying K current compatible with the observations presented here is introduced. were voltage clamped using the single sucrose gap technique (Morad & Orkand, 1971). The general procedure is described in detail in the previous paper (Cleemann & Morad, 1978).…”

Contractility of the Frog Ventricular Myocardium in Sodium-free Lithium Solution

“…If the magnitude of twitch contraction is determined solely by Ca ions flowed into the sarcoplasm across the membrane during action potential, that is by slow inward Ca current, the relaxation should start at the time point of repolarization as occurred in the normal Ringer, because the rate of tension development is fairly rapid even in the Li Ringer. The existence of a close relationship between the membrane repolarization and the onset of relaxation of myocardial contraction has been repeatedly demonstrated (MoRAD and TRAUTWEIN, 1968;KAWATA et al, 1969;MORAD and ORKAND, 1971).…”