The Dependence of the Strength of Sodium‐depletion Contractures of Isolated Frog Atrial Trabeculae on the Membrane Potential

Abstract

SUMMARYWhen the Na bathing isolated frog atrial trabeculae voltage clamped at -80 mV is reduced, a strong contracture develops. Upon return to normal extracellular Na concentration ([Na]0) this contracture rapidly relaxes. Hyperpolarization of the membrane by a voltage-clamp pulse during the low-Na contracture produces a rapid relaxation and the extent of this relaxation is dependent upon the size of the hyperpolarizing pulse. The membrane potential at which tension is relaxed to a constant level during low-Na perfusion, is exponentially related to the change in the Na gradient. This relationship shows that changes in the Na gradient, across the cell membrane, have nearly three times more effect on the generation of tension than changes in membrane potential. This would be consistent with the notion that contracture tension is determined by an electrogenic Na/Ca exchange across the cell membrane with a coupling ratio approaching 3 Na+/Ca2+. Exposure of the muscle to strophanthidin reduces the size of the hyperpolarizing pulse required to relax completely the low-Na contracture. As a consequence the apparent coupling ratio is increased to just above 3 Na+/Ca2 . Upon repolarization to -80 mV in low-Na Ringer solution, the redeveloped tension may be larger than that recorded immediately before the hyperpolarizing pulse. This after-effect suggests that hyperpolarization of the membrane may reduce the fall in intracellular [Na] that normally occurs when the bathing [Na] is reduced.

The Negative Inotropic Effect of Raised Extracellular Potassium and Caesium Ions on Isolated Frog Atrial Trabeculae

“…As noted previously, the application of hyperpolarizing pulses may produce a relaxation in resting tension (Chapman & Rodrigo, 1986 clamped at -80 mV was followed using an Na+-sensitive micro-electrode. The ionsensitive micro-electrode was first inserted into a cell, flow in the sucrose streams was then begun and the membrane potential clamped at -80 mV.…”

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

“…Secondly, with respect to the resting membrane potentials of -100 to -70mV associated with the K+ effect on the regular contraction, reports on the electrical control of mechanical restitution seem to be at variance (Beeler & Reuter, 1970;Lipsius et al, 1982). Potentials negative to -70mV did not alter or only slightly altered the contraction after a priming event although the Na' withdrawal contracture of frog atrial trabeculae depended on the membrane potential (Chapman & Rodrigo, 1986). At presence, therefore, the question regarding a conceivable effect of the resting membrane potential on the regular contraction by interfering with the sarcoplasmic Ca2+ concentration and its precise mechanism seems to be unsettled.…”