{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T21:04:55Z","timestamp":1778274295248,"version":"3.51.4"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1973,7,1]],"date-time":"1973-07-01T00:00:00Z","timestamp":110332800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1973,7]]},"abstract":"<jats:p>1. Insulin increased the rate of net Na extrusion from Na\u2010loaded frog skeletal muscle into glucose\u2010free Na\u2010Ringer. After a 90 min period of efflux, the insulin\u2010treated 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<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>, even though there was no definite effect upon net K flux. In spite of the decrease in intracellular water, [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub> was lower in those muscles treated with 500 m\u2010u. insulin\/ml. than in the controls.<\/jats:p><jats:p>2. Insulin consistently increased <jats:sup>22<\/jats:sup>Na efflux into Na\u2010Ringer containing either 10 or 2\u00b75 m\n<jats:sc>M<\/jats:sc>\u2010K<jats:sup>+<\/jats:sup>. This effect was reversible and was not produced by other proteins.<\/jats:p><jats:p>3. Acetylstrophanthidin (5 \u00d7 10<jats:sup>\u22126<\/jats:sup> \n<jats:sc>M<\/jats:sc>) blocked all or nearly all net Na efflux even in the presence of insulin. The presence of this concentration of acetylstrophanthidin or of K\u2010free Na\u2010Ringer inhibited the effect of insulin upon <jats:sup>22<\/jats:sup>Na efflux from Na\u2010loaded muscles.<\/jats:p><jats:p>4. All of the above results indicate that insulin in some way increases the activity of the Na pump. The inhibition by K\u2010free Na\u2010Ringer also suggests that this is not due to production of additional pump sites.<\/jats:p><jats:p>5. Insulin also increased <jats:sup>22<\/jats:sup>Na efflux and net sodium efflux into Li\u2010Ringer. When the new steady\u2010state was reached after addition of insulin, the <jats:sup>22<\/jats:sup>Na kinetics still obeyed a power relation to intracellular <jats:sup>22<\/jats:sup>Na. However, in every single case, insulin resulted in a decrease of approximately 18% in the exponent, <jats:italic>n<\/jats:italic>.<\/jats:p><jats:p>6. Curve\u2010fitting of the kinetic data to equations based upon a three\u2010site model of the Na pump suggests that insulin increases the affinity of the sites toward Na<jats:sup>+<\/jats:sup>. In terms of Eisenman's theory of ion selectivity, this would indicate an increase in the anionic field strength of the Na\u2010carrying sites and also predict that the increase in affinity for H<jats:sup>+<\/jats:sup> would be greater than that for Na<jats:sup>+<\/jats:sup>. This latter prediction is entirely consistent with the observed decrease in <jats:italic>n<\/jats:italic>.<\/jats:p><jats:p>7. The results suggest that insulin may be increasing H<jats:sup>+<\/jats:sup> efflux as well as Na<jats:sup>+<\/jats:sup> 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.<\/jats:p>","DOI":"10.1113\/jphysiol.1973.sp010255","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T10:25:11Z","timestamp":1418984711000},"page":"23-45","source":"Crossref","is-referenced-by-count":92,"title":["Effect of insulin upon the sodium pump in frog skeletal muscle"],"prefix":"10.1113","volume":"232","author":[{"given":"Richard D.","family":"Moore","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1973,7]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1973.sp010255","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1973.sp010255","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,8]],"date-time":"2023-11-08T13:08:46Z","timestamp":1699448926000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1973.sp010255"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1973,7]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1973,7]]}},"alternative-id":["10.1113\/jphysiol.1973.sp010255"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1973.sp010255","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1973,7]]}}}