HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Moore, R. D. Search for Related Content PubMed PubMed Citation Articles by Moore, R. D.

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 ²²Na 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 ²²Na 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 ²²Na efflux and net sodium efflux into Li-Ringer. When the new steady-state was reached after addition of insulin, the ²²Na kinetics still obeyed a power relation to intracellular ²²Na. 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.