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The Journal of General Physiology, Vol 48, 957-972, Copyright © 1965 by The Rockefeller University Press

ARTICLE

Cat Heart Muscle in Vitro

VIII. Active transport of sodium in papillary muscles



Ernest Page 1 and S. R. Storm 1

1 From the Biophysical Laboratory, Harvard Medical School, Boston.

Dr. Page's present address is the Department of Zoology, University of California at Los Angeles. His permanent address is Departments of Medicine and Physiology, University of Chicago

The cells of cat right ventricular papillary muscles were depleted of K and caused to accumulate Na and water by preincubation at 2–3°C. The time courses of changes in cellular ion content and volume and of the resting membrane potential (Vm) were then followed after abrupt rewarming to 27–28°C. At physiological external K concentration ([K]o = 5.32 mM) recovery of cellular ion and water contents was complete within 30 minutes, the maximal observable rates of K uptake and Na extrusion (Deltammol cell ion/(kg dry weight) (min.)) being 3.4 and 3.6, respectively. The recovery rate was markedly slowed at [K]o = 1.0 mM. Rewarming caused Vm measured in cells at the muscle surface to recover within from <1 to 9 minutes, but only slight restoration of cellular ion contents (measured in whole muscles) had occurred after 10 minutes. Studies of recovery in NaCl-free sucrose Ringer's solution made it possible to separate the ouabain-insensitive outward diffusion of Na as a salt from a simultaneous ouabain-sensitive Na extrusion which is associated with a net cellular K uptake. A hypothesis consistent with these observations is that rewarming may activate a ouabain-sensitive "electrogenic" mechanism, most probably the net active transport of Na out of the cell, from which net K uptake may then follow passively.

Submitted on December 21, 1964


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