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[Electromyographic study of 2 cases of hypopotassemia and alkalosis].
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A simple after image method demonstrating the involuntary multidirectional eye movements during fixation.
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The elongation of myofibrils from the indirect flight muscle of Drosophila.
Myofibrils which lengthen by several per cent in the presence of ATP and magnesium ions were prepared by teasing indirect flight muscle of Drosophila in solutions containing ethylenediaminetetraacetate. A study was made of the hydrogen ion, magnesium ion, ATP, and potassium chloride concentrations with which this effect could be observed. The lack of elongation with pyrophosphate and several nucleoside triphosphates suggests that the lengthening is ATP specific. A relaxing factor system comparable to that described for rabbit muscle was not demonstrable, as elongated fibrils did not shorten with calcium ions, carnosine, or digitonin.
Electron microscopical study of skeletal muscle during isotonic (afterload) and isometric contraction.
Bundles of the curarized semitendinosus muscle of the frog were fixed during isotonic (afterload) and isometric contraction and the length of the A and I bands investigated by electron microscopy. The sarcomere length, during afterload contraction initiated at 25 per cent stretch, varied depending on the afterload applied between 3.0 and 1.2 micro, i.e. the shortening amounted to 5 to 50 per cent. The shortening involved both the A and I bands. Between a sarcomere length of 3.0 to 1.7 micro (shortening 5 to 35 per cent) the A bands remained practically constant at about 1.5 micro (6 to 8 per cent shortening); the length of the I bands decreased from 1.4 to 0.3 micro (80 per cent shortening). Below a sarcomere length of 1.7 to 1.2 micro the A bands shortened from 1.5 to 1.0 micro (from 6 to 8 to 25 per cent). At sarcomere lengths 1.6 to 1.2 micro the I band was replaced by a contraction band. During isometric contraction the A bands shortened by about 8 to 10 per cent; the I bands were correspondingly elongated.
The effect of electrolytes on the contractile elements of muscle.
The effects of changes in electrolyte concentration on muscles which had been preserved in 50 per cent glycerol or washed in water were studied. The psoas preparation of Szent-Györgyi was generally used, but smooth and cardiac muscle gave the same results. If the preparations are immersed in 0.16 molar NaCl or KCl and if the electrolyte subsequently is washed out with distilled water, tension rises. This effect is not obtained if solutions of CaCl(2) or MgCl(2) are used, but it is restored by brief immersion in NaCl or KCl solutions. Changes in pH have no effect. It is concluded that divalent cations are bound more firmly than monovalent ions, but that divalent exchange with monovalent ions. After the application of ATP washing out electrolytes produces a much larger and more rapid rise in tension. This effect persists after ATP has been washed out and seems to be due to the removal of a substance which diminishes the dissociation of bound cations. Washing out electrolytes also causes a large increase in transparency and swelling. These effects are also enhanced by previous application of ATP and are abolished or diminished by divalent cations. The rise in tension and the swelling are explained as the result of an increase in the charge of the polar groups of the proteins. Because this mechanism produces only a small degree of shortening, it does not explain normal contraction, but it may be a part of this process. The significance of the phenomena described in relation to recent theories of the mechanism of muscular contraction is discussed. The observations show that increase in the charge of the contractile proteins causes contraction, not relaxation, as has been commonly assumed.
The role of phosphocreatine and adenosinetriphosphate in muscular contraction.
In the presence of 20 mM PC a strong contraction is produced in glycerol-extracted muscle fibers by ATP and AMP in concentrations as low as 10(-6)M per liter. At low concentrations of nucleotide tension rises very slowly. This rise is interpreted as being due to absorption of nucleotide by the contractile elements. AMP gives an S-shaped tension curve, indicating that the conversion of AMP into ATP is an autocatalytic process. Tension is maintained in a contracted muscle even in PC solutions free of ATP. PC alone produces a contraction if applied within 5 minutes after ATP has been washed out from a contracting muscle. It is concluded from these results that PC is the substrate for the enzymatic activity of the contractile elements and that this activity depends on the presence of bound nucleotide which acts as an energy transfer mechanism. PC accelerates relaxation which is caused by ATP under certain conditions. In the presence of PC even very low concentrations of ATP can produce relaxation. A strong contraction can be produced under these conditions by the addition of Ca ions. These observations support the conclusion that relaxation depends on the rephosphorylation of nucleotide bound by the contractile elements.
Relaxation in extracted muscle fibers.
1. Ethylenediamine tetraacetic acid (EDTA) in low concentrations imitates all the known effects of the relaxation factor ("Marsh factor"). In extracted muscle fibers which have contracted in a solution containing adenosinetriphosphate (ATP), the addition of EBTA causes relaxation, the subsequent addition of CaCl(2), contraction. 2. In fibers which have been briefly immersed in 5 MM EDTA, ATP causes rapid relaxation if Mg is also present. These fibers have essentially the same properties as briefly extracted fibers. Brief immersion into a solution containing CaCl(2) restores at once the original condition. It is concluded that EDTA produces its action by firmly combining with bound Ca, thereby inactivating it. 3. In relaxed muscle fibers not only Ca, but also lowering the concentration of Mg below a critical level, causes contraction. In such fibers Mg in the lowest effective concentrations increases contraction, but the effect reverses above a certain concentration. 4. At 0 degrees Mg in the presence of ATP has a relaxing effect without the relaxation factor. 5. The results indicate that Mg has two distinct effects in the presence of ATP. It causes contraction at low concentrations, but above a critical concentration its relaxing action prevails. The last of these effects is blocked by bound Ca. If the latter is inactivated by EDTA, Mg in sufficiently high concentrations causes relaxation. The action of the relaxation factor can similarly be explained by assuming that it acts as a complexing agent which inactivates bound Ca. 6. Previous evidence that the relaxed state depends on the formation of an enzymatically inactive ATP-protein complex was confirmed. It was found that PP in low concentrations strongly increases the relaxing effect of ATP in briefly extracted fibers.
Binding of calcium and magnesium by the contractile elements.
Using a technique for determining Ca and Mg based on Schwarzenberg's method of titration with ethylenediamine tetraacetic acid (EDTA), it was found that glycerol-extracted muscle fibers contain on the average 0.58 millimole Ca and 0.55 millimole Mg per kg. muscle. The fibers take up additional Ca or Mg from dilute solutions of these metals, but in KCl solutions, the excess is exchanged for K ions. Inorganic pyrophosphate (PP) removes part of the bound Mg, no Ca; EDTA removes predominantly Ca, but never more than about one-half the total amount. These results are discussed in relation to previous observations on the effects of PP and EDTA on mechanical properties and contractility of extracted muscle fibers. After the partial loss of bound divalent metals, muscle fibers swell in dilute salt solutions; they also contract slightly and become more translucent.
The relations between prepotential, resting potential, and latent period in frog muscle fibers.
1. Prepotentials and action potentials were recorded from amphibian striated muscle fibers. Intracellular electrodes were used for stimulating and recording. The resting potential was varied from 55 to 120 mv. by alterations of the KCl concentration of the Ringer's fluid. The magnitude of the prepotential at the initiation of the spike potential was measured and compared to the resting potential and the latent period (time between stimulus "make" and excitation). The magnitude of this prepotential varied with the resting potential. 2. A large prepotential or cathodal depolarization was required to excite a fiber with a high resting potential. If a fiber with a high resting potential fired late (long latency), the adequate prepotential was larger than if the fiber fired early. Fibers with low resting potentials had smaller adequate prepotentials. Also, the adequate prepotential was independent of the latent period, in these depolarized fibers. 3. If the concentration of Ca(++) was increased tenfold, the adequate prepotential of depolarized fibers became strongly dependent upon the latency. 4. Fibers with large or normal resting potentials were prone to respond repetitively during the passage of long duration shock, whereas depolarized and Ca(++)-treated fibers were not. 5. The so-called critical membrane potential (which is defined as the transmembrane potential at the point of excitation) was not independent of the resting potential.
The non-correlation of bioelectric potentials with ionic gradients.
The sartorius muscles of 320 toads have been analyzed for Na(+) and K(+). There is a wide variation in the Na(+) content which when calculated intracellularly varied from 0 m.eq./kg. to 58 m.eq./kg. In particular it was found that the distribution of internal Na(+) in the intact animal was such that only 17 per cent of the muscles should give from the Nernst equation the observed overshoot of 37 mv. In contrast to this wide variation the K(+) content is comparatively constant, the range being 71 to 112 m.eq./kg. The mean observed resting potential of 87 mv. agreed well with the potential calculated from the mean intracellular K(+) by the Nernst equation. Analyses of plasma show that the Na(+) content is constant at 130 m.eq./liter, and the K(+) is 3.0 m.eq./liter. The resting and action potentials of 77 muscles have been recorded and then the muscles have been analyzed. The results have shown that there is no correlation between the level of intracellular Na(+) and the overshoot. Furthermore the apparent correlation between the average K(+) content and the average resting potential has been shown to be fortuitous, when the correlation in individual muscles is considered. When a muscle is soaked in Ringer solution for several hours there is a gain of Na(+) and a loss of K(+). These shifts should result in changes in the respective potentials, but such changes were not found. The above findings have been discussed in the light of the present theories that the resting potential and the action potential are directly related to the ionic ratio across the membrane. Our results very definitely do not support the theory that the overshoot is related to the Na(+) gradient, and this also applies with respect to the K(+) gradient and the resting potential.
The effect of changes of environment on the electrical and ionic pattern of muscle.
The resting and action potentials of sartorius muscles of the toad, Bufo marinus, have been measured under varying conditions of external environment. At the same time, analyses for Na(+) and K(+) content were carried out. There was a slight elevation of 2 mv. when the measurements were made in phosphate-Ringer instead of in bicarbonate-Ringer. The R.P. was independent of the hydrogen ion concentration between pH 6.5 and 8.5, although at these pH's there was marked alteration in the level of Na(+) and K(+) in the muscle. Alteration of the external K(+) level between 0 and 50 m.eq./liter has little influence on the internal K(+) concentration. When the log of the external K(+) concentration is plotted against the R.P. there is not a linear relationship until the external K(+) is raised above 12 m.eq./liter, at which point the cell is unexcitable. Above this value a straight line with a slope of 58 mv. per ten-fold change in concentration is obtained, but the absolute values at any point are about 35 per cent higher than those which would be given by the Nernst equation. Alteration of the external Na(+) level within a range of 45 to 650 m.eq./liter resulted in marked changes in the internal Na(+) content, without, however, having any effect on the ratio Na(+) (out)/Na(+) (in). This ratio has remained at about 3 in spite of marked fluctuations in the absolute value of the internal and external Na(+) levels. When the Na(+) level is lowered there is a decrease in the height of the action potential although there is no alteration in the ratio Na(+) (out)/Na(+) (in). As the Na(+) level is raised the height of the action potential is not affected even in the presence of a fivefold increase in Na(+) in the Ringer. The results do not support the conclusion that the bioelectric potentials can be calculated from the ionic ratios by means of simple physical chemical hypotheses such as the Nernst or Goldman equations. The maintenance of the normal K(+) content of the cell cannot be accounted for by a Donnan mechanism. No definite evidence has been produced to explain the mechanism of a Na(+) "pump." In other words, the concept of a Na(+) pump requires that there shall be a physico- or organochemical mechanism which will distinguish between Na(+) and K(+) (or other) ions. There is evidence that Na(+) can be extruded against a concentration gradient. On the other hand the cell is able to maintain a constant ratio of external to internal Na(+) even when the cell has been severely damaged by very high external Na(+) levels.
The effectiveness of the longitudinal field, coupled with depolarization in activating frog twitch muscles.
EFFECTIVE EXCITATION, PRECEDING THE MECHANICAL RESPONSE IN FROG TWITCH MUSCLES, INVOLVES TWO DISTINCT EVENTS: depolarization of the excitable membrane and the flow of internal currents. To distinguish between the effects of these two potential factors in activation of the contractile machinery, experiments ought to be conducted in which one or the other is excluded. Our experiments are designed to distinguish between these effects by indirect methods. Depolarization in a longitudinal electric field can be expected to be greatest at the ends where current leaves the muscle fibers (space constant at [K] = 16 mM/liter is >1 mm.), whereas the internal longitudinal current is known to be greatest in the middle portion. Depolarization, therefore, should affect the ends more strongly and internal current the middle portion. Our experiments show that non-propagating frog twitch muscles shorten, during isotonic work, along their whole length and not only at their ends, when effectively stimulated in a longitudinal A.C. field. At a field strength about twice the new threshold value (at [K](o) = 16 mM) shortening is distinctly greater in the middle portion of the muscle than at the ends. The muscles, although temporarily non-propagating, remain intact throughout the experiment, as demonstrated by complete recovery after repolarization. These findings may be taken as an indication that internal currents are more directly linked to activation than is depolarization, but the latter is an essential priming step, which must precede or coincide with effective current flow.
The effect of enzyme inhibitors on the resting potential and on the ion distribution of the sartorius muscle of the frog.
Isolated frog sartorii were exposed for 30 minutes to HETP-an irreversible anti-cholinesterase, and were then soaked in Ringer's at 15 degrees C. for 16 hours. At the end of the period of soaking the mean resting potential of the muscle fibers was only 29 mv. The decrease in the resting potential of the HETP-treated muscles was accompanied by a loss of potassium and a gain in sodium by the muscles. The effect of anticholinesterases on sodium extrusion was studied by incubating the muscles in a Ringer's containing half of the normal amount of sodium. The muscles respond by extruding sodium against a concentration gradient into the external medium. Sodium extrusion was blocked by prior exposure of the muscle to HETP, and reversibly blocked by exposure to physostigmine. The inhibition of sodium extrusion by physostigmine was correlated with the inhibition of the intracellular cholinesterase. Sodium extrusion was also blocked by high concentrations of 2-methyl-1,4-napthaquinone 8-sulfonic acid and by alpha-ketoglutarate, which are known to inhibit choline acetylase in vitro. But sodium extrusion was not affected by a third inhibitor of choline acetylase, phenobarbital. Sodium extrusion was unaffected by KCN and partially blocked by IAA. The IAA block was eliminated by the addition of pyruvate. It is concluded that either glycolysis or oxidative metabolism can furnish the energy needed for sodium extrusion.
The effect of ions upon the response of smooth muscle to cooling.
The slow tonic responses of the anterior byssus retractor of Mytilus edulis to rapid cooling were investigated by simultaneously recording tension and resting potential changes after soaking the muscle in banthine, a powerful neuromuscular blocking agent. The quantitative relations between the amount of cooling and the amount of associated depolarization necessary for contraction at various concentrations of potentiating potassium can be expressed in a family of curves. The plateaus of the curves for sea water and for potassium-free sea water were beneath the depolarization value necessary for contraction, so that it is clear that no amount of cooling with sea water alone or with potassium-free sea water would ever be effective. When the muscle is treated with subthreshold amounts of potassium and rapidly cooled in various concentrations of sodium ion and calcium ion, respectively, the sodium and calcium do not affect the amount of depolarization. Acetylcholine, in subthreshold amounts, has a potentiating effect, but, unlike potassium and cooling, acts through the nervous apparatus. Mytilus muscle will respond to cooling with tonic contraction whenever a critical threshold amount of depolarization is achieved. Cooling alone cannot trigger the contraction since it cannot bring about sufficient depolarization. Cooling can result in contraction, however, if used in conjunction with some other subthreshold depolarizing agent. Cooling affects the contractile mechanism by first causing membrane breakdown and depolarization.
Active state of muscle in iodoacetate rigor.
Frog sartorius muscles, equilibrated to 2 x 10(-4)M iodoacetic acid-Ringer's solution and activated by a series of twitches or a long tetanus, perform a rigor response consisting in general of a contractile change which plateaus and is then automatically reversed. Isotonic rigor shortening obeys a force-velocity relation which, with certain differences in value of the constants, accords with Hill's equation for this relation. Changes in rigidity during either isotonic or isometric rigor response show that the capacity of the rigor muscle to bear a load increases more abruptly than the corresponding onset of the ordinarily recorded response, briefly plateaus, and then decays. A quick release of about 1 mm. applied at any instant of isometric rigor output causes the tension to drop instantaneously to zero and then redevelop, the rate of redevelopment varying as does the intensity of the load-bearing capacity. These results demonstrate that rigor mechanical responses result from interaction of a passive, undamped series elastic component, and a contractile component with active state properties like those of normal contraction. Adenosinetriphosphate is known to break down in association with development of the rigor active state. This is discussed in relation to the apparent absence of ATP splitting in normal activation of the contractile component.
The control of membrane ionic currents by the membrane potential of muscle.
Comparisons between electrotronic potentials and certain predicted curves allow the identification of the membrane potential at which the sodium and potassium currents are switched on in frog sartorius. The activation potentials (the membrane potentials at which the ionic currents are great enough to be resolved by the method) are functions of the resting potential and time but not of ionic concentration. In the normal fiber, the activation potential for sodium lies nearer the resting potential and depolarizations set off sodium currents and action potentials. Below a resting potential of 55 to 60 mv. sodium activation is lost and conduction is impossible. A tenfold increase of calcium concentration lowers (moves further from the resting potential) the sodium activation potential by 20 to 25 mv. whereas the potassium activation potential is lowered by only 15 mv. Certain consequences of this are seen in the behavior of the muscle cell when it is stimulated with long duration shock.