The tension‐depolarization relationship of frog atrial trabeculae as determined by potassium contractures.

Abstract

SUMMARY1. In the presence of extracellular Na ions K contractures evoked from isolated frog atria1 trabeculae show an initial phasic and a subsequent tonic contractile response.2. The phasic response shows a steep dependence on membrane potential, persists in Na-free fluid, but is blocked by Mn ions, D600 and tetracaine. It has an indirect dependence on the [Ca]0 and would seem to be associated with both the secondary inward current and the release of Ca2+ from intracellular stores.3. The tonic component of the K contracture is unaffected by D600 or tetracaine, shows a shallow dependence on membrane potential but is absent in Na-free fluid. Its tension-depolarization curve is immediately affected by alteration of either the [Ca]

The effects of tetracaine on the membrane currents and contraction of frog atrial muscle.

“…1 B and 3B) agrees well with the results obtained with K contractures (Chapman & Tunstall, 1981). The quantitative dependence of both the phasic and tonic components of contraction upon membrane potential as determined by the two methods also show a marked similarity.…”

“…Again, in the presence of tetracaine, the initial phase of tension development is slowed and the slow inward current is inhibited, while the maximum tension is reduced, the final level of the plateau tension is increased. These changes in contractile response are also seen with K contractures on the same tissue (Chapman & Tunstall, 1981). Outward current is also reduced by tetracaine in a dose-dependent way.…”

“…Exposure to Mn2+, D600 or perfusion with Ca-free fluid containing EGTA causes a large shift in the tension-depolarization curve of frog atrial muscle in Na-free fluid and blocks the slow inward current (Einwichter et al 1972;Leoty & Raymond, 1972;Chapman & Tunstall, 1981). However, strong depolarization will still evoke a contractile response which is blocked by tetracaine.…”

“…R. A. CHAPMAN AND C. LEOTY In mammalian cardiac muscle procaine reduces the strength of the heart beat and inhibits contractions evoked in Na-free fluid by electrical depolarization (Thorens, 1971) while tetracaine antagonizes contractures induced by the application of caffeine (Chapman & Leoty, 1976a). In amphibian heart, tetracaine and procaine inhibit the contractures initiated by caffeine, hypertonic fluids and rapid cooling in Na-free or K-rich fluids (Chapman & Miller, 1974;Chapman & Ellis, 1974;Chapman, 1978) and the phasic component ofthe K contractures (Chapman & Tunstall, 1981). Furthermore, Eisner, Lederer & Noble (1979) have noted that tetracaine also blocks the slow inward current in mammalian Purkinje fibres.…”

The control of the contraction of myocytes from guinea‐pig heart by the resting membrane potential

“…Negative inotropic effects (Reiter et al, 1971), presumably related to Na'-pump activation and alterations of the action potential, and transient increases of contraction (Kavaler et al, 1972), however, indicate the diversity of K+ actions. The reversal from a negative to a positive inotropic effect of K+ after reduction of extracellular Na+ in guinea-pig papillary muscle (Ebner & Siegl, 1986) and the role of K+ in the inotropic response to intracellular Na+ (Ebner et al, 1986) could suggest a control of the contraction by the resting membrane potential via Na'-Ca2+ exchange in a way which resembles the effect of high K+ concentrations in frog atrial trabeculae on the Na' withdrawal contracture (Chapman & Tunstall, 1980) or the Na'-dependence of the K+-induced contracture (Chapman & Tunstall, 1981). The influence of high K+ concentrations on Ca2+ fluxes (Busselen, 1982) or intracellular Ca2+ ) is in line with the contracture experiments.…”