ABSTRACT
Most early work on cold sensitivity of mammalian cells centered on the idea that Adenosine triphosphase (ATP) was limiting and that cold adaptation had to consist of better metabolic function at low temperature. By this argument the sodium Na-K pump would fail in cold-sensitive cells because of lack of ATP to fuel it. In addition to the difference in response to temperature there was also a difference in the pattern of ATP dependence of the Na-K pump even at 37°C in red cells of ground squirrels and guinea pigs. In cold-sensitive cells, cooling inhibits the Na-K pump more than it does the various pathways for passive entry of Na and loss of K. Na entry is insufficiently reduced with cooling in cold-sensitive guinea pig red cells because the Na-H exchange pathway is both activated and uncoupled by cooling. In a cold-tolerant cell, shutdown of Mg2+ transport might contribute to a rise of free cytoplasmic Mg2+.
