Prinfrd in (.S..4. EFFECT OF INSULIN ON POTASSIUM EXCHAN(;E IN NORMAL AND OUABAIN-TR.EATED SKELETAL MUSCLE

It has long been known that insulin in the presence of lactate causes a net increase in the [K] of isolated frog muscle (Manery et cl., 1950). Further study has shown that the add!-tional uptake of K in the presence of insulin occurs without the addition of lactate (Manery et al., 1956) and is not related to the con-comitant stimulation of the oxygen consump-tion by insulin (Smillie and Manery, 1960; Gourley, 1961). The possibility remains that insulin directly affects the processes responsible for the maintenance of muscle K]. The mechanism by which the muscle fiber maintains its [K] at a level many times that of the extracellular fluid is still incompletely under-stood. Under normal conditions, the gradient between the intracellular and extracellular [K] is consistent with the polarity and the size of the membrane potential as given by the Nernst equation. Thus the discovery that insulin in-creased the resting membrane potential of skeletal muscle (rat) led Zierler (1959) to sug-gest a causal relationship between this effect and the increase in muscle [K] which followed. An alternative but not necessarily exclusive explanation for the distribution of muscle K is that K ions are actively transported into muscle fibers by means of specific carrier mole-cules and leave the fibers by diffusion down the concentration gradient (Gourley, 1964a). In a previous paper (Gourley, 1964b), the net loss of K which occurs when an isolated skeletal muscle is exposed to ouabain was explained in terms of competition between the glycoside and K for the K carrier molecules. Zierler (1960) concluded that insulin decreased both the influx and the effiux of K from rat muscle, the effect on efflux being greater by an amount sufficient Received for publication November 23, 1964