Abstract
How can cells maintain high K+/low Na+ interiors while exposed to low K+/high Na+ environments? A major concern from the late 1930s and through the following decade—the period considered here—was to distinguish between alternative models for explaining that perplexing asymmetry. This chapter describes studies on muscle. The next two chapters deal with studies carried out simultaneously on red blood cells and nerve cells—in some cases by the same individuals and for similar purposes, in some cases by other investigators with quite different interests.
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Notes to Chapter 3
Fenn (1936).
Although the ionic radius of K+ is larger than that of Na+ and Cat+, the hydrated radius is smaller. The assumption was that hydrated ions are the species that cross.
Fenn (1936), p. 462.
Fenn et al. (1934); Mond and Netter (1932).
Mond and Netter (1932). This possibility was explicitly examined by Manery et al. (1938) who concluded that proteins of the extracellular connective tissue could not represent the binding site for “excess” Na+.
Fenn and Cobb (1936).
Ibid., p. 354.
Fenn (1936), p. 464.
Ibid., p. 451.
Ibid., p. 451. Earlier, Fenn et al. (1934) concluded that “it seems necessary to assume complete impermeability to either anions or cations in order to explain the retention of potassium” (p. 271); the possibility of secretion was not even raised.
Dean (1987) considered in retrospect that “pumps were unpopular because no one could imagine how they might work,” and “no possible compound of sodium… was sufficiently different from the corresponding potassium compound” to provide the necessary selectivity; moreover, “physical chemists were confident that they could explain the results of all reactions by equilibrium theory” (pp. 451, 453, 454).
Conway and Boyle (1939); Boyle and Conway (1941). To eliminate uncertainty arising from alphabetic listings of authors in the Journal of Physiology,the paper specified that the “theoretical plan of the research is due to the senior author” (p. 62); in case someone might be uncertain about who was senior author, Conway later stated that “the theoretical part… was due to the present author” (1960, p. 26).
Conway et al. (1939); Manery and Hastings (1939); Heppel (1939); Boyle et al. (1941).
Boyle and Conway (1941), p. 44.
Ibid., p. 8.
Heppel (1939).
Heppel and Schmidt (1938). Heppel planned such experiments in Rochester, but, locked into the progression of medical school, he ran out of time.
Heppel (1940).
Hahn et al. (1939).
Ibid., p. 1556.
Hevesy and Rebbe (1940).
Griffiths and Maegraith (1939), p. 160. They did not mention muscle.
Greenberg et al. (1940).
Manery and Bale (1941), pp. 229–230.
Ibid., p. 224.
Steinbach (1940a).
Ibid., p. 700.
Steinbach (1940b), p. 244.
Ibid., p. 244.
Ibid., p. 251.
Ibid., p. 251.
Steinbach (1941), p. 63. He cited Burton’s 1939 paper discussing steady states in biological systems, who in turn acknowledged A. V. Hill’s seminal contributions.
Steinbach (1947), p. 870.
Dean, in Steinbach (1940b), p. 252.
Dean (1941), p. 333.
Dean (1941). This was in a relatively obscure journal, which, coupled with the disruptions caused by the war, contributed to Dean’s paper being overlooked by many researchers. Distribution of Na+ and K+ in Muscle
Ibid., pp. 344–345.
Ibid., pp. 346–347.
Ibid., p. 347.
Krogh (1946).
Ibid., p. 140.
Ibid., p. 180.
Ibid., p. 183.
Ibid., p. 188.
Fenn (1940).
Ibid., p. 378.
Ibid., p. 378.
Ibid., p. 403.
Fenn (1941), p. 7.
Ibid., p. 7.
Fenn et al. (1944), p. 75.
Conway (1945).
This is Mond and Netter’s proposal, coupled with permeability to Nat
Conway (1945), p. 70.
Ibid., p. 70. What Manery and Bale said was: “The most reasonable explanation at the moment is that sodium has penetrated muscle fibre membranes hitherto believed impermeable to it” (1941, p. 224).
Conway (1946).
Ibid., p. 717.
Ibid., p. 715.
Ibid., p. 715.
Ibid., p. 715.
Access to radioisotopes was limited not only by few institutions having cyclotrons to produce those isotopes but also by the short half lives of 42K (12 hours) and 24Na (15 hours), which made transport to distant locales impossible.
Particularly significant in this estimation are the number of assumptions: that weight gains parallel the K+ gains; that soaking muscles in media containing only 2.5 mM K+ has no deleterious effects (in contrast to Conway’s earlier studies); that changes in bathing solutions do not affect permeability; that K+ enters with Cl as a neutral species (so that membrane potentials would not affect influx); etc.
Another assumption in his calculations is that all energy production is by oxidative means. Conway showed that adding cyanide (an inhibitor of oxidative metabolism) did not affect Na+ movements (assessed as weight changes), but he did not cite the paper by Dean (1940) showing that both aerobic and anaerobic metabolism in frog muscle must be inhibited before changes in ion content occurred.
Conway (1946), p. 716.
Ibid., p. 716.
Ibid., p. 715.
Conway (1947a,b).
Conway and Hingerty (1948).
Conway (1947a), p. 598.
Conway et al. (1946).
Steinbach and Spiegelman (1943), p. 195; Steinbach (1944).
Steinbach (1951).
Keynes (1949b). Support for Steinbach’s results is confined to a statement that Steinbach’s “experiments… have recently been confirmed” (p. 169), with the citation of “Keynes,… unpublished observations.”
Steinbach (1951), p. 287.
Wilde (1945).
Darrow (1944), p. 117. He cited four published replications.
Wilbrandt (1947).
Ussing (1947); Levi and Ussing (1948).
Peculiarly, Ussing (1980, p. 7, and 1994, p. 92) described these calculations as indicating that far more energy seemed to be required for pumping than frog muscles could generate.
Ussing (1947). He imagined a “particle” in the membrane that may face the interior of the cell and there bind a Na’ in the cytoplasm. Then, by random thermal movement in the membrane, this particle may reorient to face the exterior of the cell where the transported Na+ is released. A Na’ from the extracellular medium may then bind for the reverse trip. If all Na’ in the cytoplasm is labeled initially, that labeling will eventually be equally distributed by such a mechanism, even though there is no net movement of Na’.
Harris and Burn (1949).
Harris (1950).
Steinbach (1952).
Ibid., p. 454.
Biographical information is from interviews, reminiscences (Ussing, 1980, 1994; Dean, 1987), and biographies (Maizels, 1969; Schmidt-Nielsen, 1995).
Krogh reported that experiments in Copenhagen using radioactive isotopes, begun in the winter of 1943, “had to be suspended during December and January owing to the seizure of the Institute for Theoretical Physics” (Holm-Jensen et al., 1944, p. 3).
Hahn and Hevesy (1941), pp. 60–61. They listed four possibilities: (1) K+ cannot cross the membrane; (2) K+ is constrained from leaving the cell by electrical forces; (3) K+ is constrained from leaving by binding to constituents within the cell; and (4) the constant loss from the cell is balanced by an equivalent secretion into the cell.
Maizels (1969, p. 76) commented that “Steinbach’s results are in fact easily reproducible [and] ultimately Conway accepted the reality of active and passive sodium fluxes.”
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© 1997 American Physiological Society
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Robinson, J.D. (1997). Accounting for Asymmetric Distributions of Na+ and K+ in Muscle. In: Moving Questions. People and Ideas Series. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7600-9_3
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