Experimental Physiology
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Quarterly Journal of Experimental Physiology 71.4 pp 675-687
© The Physiological Society 1986
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THE DEPENDENCE OF THE STRENGTH OF SODIUM-DEPLETION CONTRACTURES OF ISOLATED FROG ATRIAL TRABECULAE ON THE MEMBRANE POTENTIAL

R. A. Chapman 1 and Glenn C. Rodrigo 2

1 Laboratory of Cellular Cardiology, Department of Physiology, The Veterinary School, Park Row, University of Bristol, Bristol BS1 5LS
2 Department of Physiology, University of Leicester, Leicester LE1 7RH

When 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]o) 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.

Submitted on January 15, 1986







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Copyright © 1986 by the The Physiological Society.