Abstract
In the presence of extracellular Na+ K contractures evoked from isolated frog atrial trabeculae show an initial phasic and a subsequent tonic contractile response. The phasic response shows a steep dependence on membrane potential, persists in Na-free fluid, but is blocked by Mn2+, D600 [.alpha.-isopropyl-.alpha.-[(N-methyl-N-homoveratryl)-.gamma.-aminopropyl]-3,4,5-trimethoxyphenylacetonitrile] and tetracaine. It has an indirect dependence on the [Ca]0 and seems to be associated with both the secondary inward current and the release of Ca2+ from intracellular stores. The tonic component of the K contracture is unaffected by D600 or tetracaine, and shows a shallow dependence on membrane potential, but is absent in Na-free fluid. Its tension-depolarization curve is immediately affected by alteration of the [Ca]0 or the [Na]0. The form of the tension-depolarization relationship and the effects of [Ca]0 and [Na]0 are consistent with the strength of the tonic tension being determined by a 3Na+ for 1Ca2+ exchange across the cell membrane. Results agree well with those obtained previously with voltage-clamp experiments on the same tissue, and may also help with the interpretation of Ca-flux experiments.