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A direct cytoplasmic connection between macrophages and potential antibody-producing cells has been demonstrated in lymph nodes and spleen. This was observed in the tissues from both immunized and nonimmunized rabbits.

1. Insulin increased the rate of net Na extrusion from Na-loaded frog skeletal muscle into glucose-free Na-Ringer. After a 90 min period of efflux, the insulin-treated muscles contained approximately 11% less intracellular water than did their controls. This decrease in intracellular water resulted in an increase in the concentration of intracellular K, [K(+)](i), even though there was no definite effect upon net K flux. In spite of the decrease in intracellular water, [Na(+)](i) was lower in those muscles treated with 500 m-u. insulin/ml. than in the controls.2. Insulin consistently increased (22)Na efflux into Na-Ringer containing either 10 or 2.5 mM-K(+). This effect was reversible and was not produced by other proteins.3. Acetylstrophanthidin (5 x 10(-6)M) blocked all or nearly all net Na efflux even in the presence of insulin. The presence of this concentration of acetylstrophanthidin or of K-free Na-Ringer inhibited the effect of insulin upon (22)Na efflux from Na-loaded muscles.4. All of the above results indicate that insulin in some way increases the activity of the Na pump. The inhibition by K-free Na-Ringer also suggests that this is not due to production of additional pump sites.5. Insulin also increased (22)Na efflux and net sodium efflux into Li-Ringer. When the new steady-state was reached after addition of insulin, the (22)Na kinetics still obeyed a power relation to intracellular (22)Na. However, in every single case, insulin resulted in a decrease of approximately 18% in the exponent, n.6. Curve-fitting of the kinetic data to equations based upon a three-site model of the Na pump suggests that insulin increases the affinity of the sites toward Na(+). In terms of Eisenman's theory of ion selectivity, this would indicate an increase in the anionic field strength of the Na-carrying sites and also predict that the increase in affinity for H(+) would be greater than that for Na(+). This latter prediction is entirely consistent with the observed decrease in n.7. The results suggest that insulin may be increasing H(+) efflux as well as Na(+) efflux and thereby may be increasing intracellular pH. It is suggested that some of the intracellular effects of insulin might be mediated by such an effect.

Measurements have been made of the fluxes of thallous ions (Tl(+)) across the membrane of frog sartorius muscle fibers. These show that at an external concentration of 74 microM the influx is about 270 x 10(-15) moles/cm.(2) sec., while the efflux from a muscle with an internal concentration equal to the above is 5 x 10(-15) moles/cm.(2) sec. The efflux is increased of the order of 300-fold during a muscle twitch, and Tl(+) reach a steady-state distribution between fiber water and Ringer solution that is very close to the corresponding ratio for K(+). High concentrations of Tl(+) depolarize the membrane about 58 mv. for a tenfold increase in external concentration. The results obtained are consistent with the view that the muscle fiber membrane cannot distinguish between the toxic heavy metal Tl(+) and K(+), provided that the concentrations of the former ion are kept low. High concentrations of Tl(+), if allowed to act for an appreciable period of time, lead to irreversible damage to muscle.