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R D Keynes

Publications and source records attributed to R D Keynes.

At least 73 records · Page 4Linked to original sources
PubMed1969

The ouabain-sensitive fluxes of sodium and potassium in squid giant axons.

1. Fifty to ninety per cent of the Na efflux from axons of Loligo forbesi is inhibited by ouabain. The properties of the ouabain-sensitive component of the Na efflux are different from those of the ouabain-insensitive component.2. In unpoisoned axons with an average Na content of 75 m-mole/kg axoplasm the bulk of the ouabain-sensitive Na efflux is dependent on external K.3. In the presence of 460 mM Na in the external medium, raising the external K concentration from 0 to 100 mM increases the ouabain-sensitive Na efflux along a sigmoid curve which shows signs of saturating at high K concentrations.4. The curve relating ouabain-sensitive K influx to external K concentration is similar in shape to that for the ouabain-sensitive Na efflux. At all K concentrations examined the ouabain-sensitive K influx was less than the ouabain-sensitive Na efflux.5. Potassium-free sea water acts rapidly in reducing the Na efflux. There is no appreciable difference between the rates of action of K-free sea water on the Na pump and Na-free sea water on the action potential.6. Caesium and Rb can replace external K in activating the ouabain-sensitive Na efflux. Both the affinity and maximum rate of the Na efflux mechanism are lower when Cs replaces K as the activating cation.7. Isosmotic replacement of external Na by either choline or dextrose, but not Li, increases the affinity of the ouabain-sensitive Na efflux mechanism for external K without appreciably affecting the maximum rate of pumping. External Li behaves like external Na and exerts an inhibitory action on the Na efflux.8. There is a large ouabain-sensitive Na efflux into K-free choline or dextrose sea waters. Addition of either Na or Li to the external medium reduces this efflux along a section of a rectangular hyperbola. The properties of this efflux suggest that there is a residual K concentration of up to 2 mM immediately external to the pumping sites in the axolemma.9. Over the range of internal Na concentrations studied (16-140 m-mole/kg axoplasm) the ouabain-sensitive Na efflux increased linearly with Na concentration.10. Tetrodotoxin (10(-6) g/ml.) reduces the Na influx by about half, but does not affect the ouabain-sensitive Na efflux.11. Isobutanol (1% v/v) reversibly decreases both the ouabain-sensitive and ouabain-insensitive components of the Na efflux.12. Application of 2 mM cyanide to axons immersed in K-free sea water produces a transient rise in the Na efflux. This rise is not seen if ouabain is included in the sea water. The rise in efflux occurs at a time when the axons are partially poisoned and contain adenosine triphosphate (ATP) but no arginine phosphate (ArgP). A similar, but maintained rise can be obtained after application of dinitrophenol (DNP) at pH 8.0. The increased Na efflux in these partially poisoned axons is also inhibited by ouabain.13. Under conditions of partial-poisoning by alkaline DNP, there is a ouabain-sensitive Na influx from K-free sea water. The ouabain-sensitive Na influx is of similar size to the ouabain-sensitive Na efflux. These results show that in partially-poisoned axons immersed in K-free sea water intracellular Na exchanges with extracellular Na in a one-for-one manner by a ouabain-sensitive route. External Li cannot replace external Na in maintaining this process.14. Axons partially poisoned with alkaline DNP are not insensitive to external K. In the absence of external Na their response to external K is essentially the same as that seen in unpoisoned axons.15. Possible mechanisms are discussed for the appearance of Na-Na exchange in partially poisoned axons.

Animals↗
PubMed1969

Light scattering and birefringence changes during activity in the electric organ of electrophorus electricus.

1. In an attempt to obtain information about structural changes related to electrical activity in Electrophorus electroplates, we have determined the size and time course of the changes in light scattering and in bire-fringence that occur during and after the discharge of the electric organ.2. The changes in light intensity detected with a photomultiplier were never greater than 0.2% for a single discharge, and were often much smaller than this, but records with an acceptable ratio of signal to noise could be obtained by signal-averaging techniques.3. A single stimulus led to a decrease, then an increase, and finally another decrease in the light scattered by slices of the main electric organ. These three phases were designated E1, E2 and E3.4. E1 started at the beginning of the action potential, and its peak was reached at the same time as the completion of repolarization, even when the repolarization was delayed by cooling or hastened by drawing larger currents from the tissue.5. E2 was proportional to the integral of the current flowing through the slice of electric organ, and may arise from the swelling and shrinking of the tubules that stud the faces of the electroplates. It developed within a millisecond or two of the start of an applied current, and lasted for about 100 msec.6. E3 was a variable decrease in scattering that lasted for some seconds.7. A stimulus also led to a transient increase in the birefringence of the electric organ. The optical change followed the change in electrical potential across the innervated faces of the electroplates with a delay of somewhat under 50 musec.8. This voltage-dependent change in birefringence may arise from a Kerr effect (electric birefringence) in the membrane or from compression of the membrane.

Action Potentials↗
PubMed1968

The origin of the initial heat associated with a single impulse in mammalian non-myelinated nerve fibres.

1. A study has been made of the temperature changes associated with the passage of a single impulse in rabbit desheated vagus nerves.2. The initial changes consist of an evolution of positive heat followed by a reabsorption of most of it; i.e. there is a phase of positive and a phase of negative heat production.3. The size of the positive heat, its time of onset, and the time of onset of the negative heat have been measured by an analogue method of analysis. In addition, these parameters, together with the size of the negative heat and the duration of both phases of initial heat, have been studied with the aid of a computer, and also by conventional heat block analysis.4. At about 5 degrees C the measured positive heat is 7.2 mucal/g. impulse. It starts as soon as the compound action potential reaches the thermopile and lasts for about 107 msec.5. This positive heat decreases with increasing temperature, the ratio of heat at 4 degrees C to that at 14 degrees C being 1.86.6. The measured negative heat at about 5 degrees C is 4.9 mucal/g. impulse. It starts 102 msec after the onset of positive heat, and lasts for about 240 msec.7. When the sodium of Locke solution is replaced by lithium the positive heat is reduced by 19%, but the negative heat is increased by 22%.8. In potassium-free solutions the positive heat is hardly affected (increase of 5%), but the negative heat is more than doubled. As a result the nerve may become briefly colder than its initial temperature by about 2 mu degrees C.9. The effect of sodium-deficient solutions on the positive heat is somewhat variable, but the negative heat is consistently diminished.10. Replacement of the chloride of Locke solution by sulphate or nitrate has little effect on the positive heat. The negative heat is reduced in size by 26% and in duration by 22%.11. Replacement of most of the sodium of Locke solution by barium reduces or abolishes the negative heat, and increases the measured size of the positive heat nearly threefold.12. Veratrine (10(-5) g/ml.) produces a nearly tenfold increase in the net positive heat.13. Ouabain (1 mM) and antimycin A (1 mug/ml.) applied for 30-60 min have little effect on the initial heat production.14. Over the temperature range 5-15 degrees C, and for the ionic solution changes described above, there is close agreement in timing between the positive heat and the rising phase of the action potential, and between the negative heat and the falling phase.15. Because of the inevitable temporal dispersion of the action potential over the face of the thermopile, the observed temperature changes are smaller than those which occur at a single point in the nerve close to a stimulating electrode. The corrected value of the positive heat at 5 degrees C is 24.5 mucal/g. impulse, while that of the negative heat is 22.2 mucal/g. impulse.16. The heats of mixing of the ions in solution that interchange during the action potential are much too small to account for the observed initial heats, but an exchange of ions associated with fixed charges might make a significant contribution to the heats.17. The condenser theory, according to which the positive heat represents the dissipation of electrical energy stored in the membrane capacity, while the negative heat results from the recharging of the capacity, appears unable to account for more than half of the observed temperature changes.18. It seems probable that the greater part of the initial heat results from changes in the entropy of the nerve membrane when it is depolarized and repolarized.

Action Potentials↗
PubMed1968

Renal excretion of potassium in the xheep.

1. Observations were made on the daily intake and excretion of potassium and sodium in sheep housed in metabolism cages and fed once daily.2. The diet of chaffed hay and crushed oats provided 400-600 m-moles K and 50-60 m-moles Na daily. About 90% of the K was excreted in the urine, and over 90% of the Na was found in the faeces.3. In two groups of three experiments on each of three sheep, the urinary responses to intra-ruminal dosing just before feeding of (i) 1 l. distilled water, (ii) 1 l. 0.25 N-KCl, and (iii) 1 l. 0.125 N-NaCl, were studied. In the first group, urine was collected via the urine/faeces separator of the metabolism cage, whereas for part of the experiments in the second group it was collected by an indwelling bladder catheter.4. In a third group of experiments with the same sheep, the effects on urinary excretion of K and Na of intra-ruminal dosing with (i) 1 l. distilled water, (ii) 1 l. 0.25 N-K acetate, and (iii) 1 l. 0.25 N-Na acetate were investigated. During part of these experiments urine was again collected via an indwelling bladder catheter. With chloride, 82% of the additional potassium was excreted in urine in the 24 hr after dosing, but with acetate only 65%. For sodium, the corresponding figures were 12-40% with chloride and 43% with acetate.5. In most experiments, the administration of K salts produced a marked kaliuresis and, in spite of the low sodium intake, a natriuresis as well, which did not usually coincide with maximum K excretion. No adequately tested explanation appears to exist for the natriuresis observed in response to treatment with K salts.

Acetates↗
PubMed1968

The components of the sodium efflux in frog muscle.

1. In normal Ringer solution containing 2.5 mM-K only 37% of the efflux of labelled sodium from a freshly dissected frog muscle is blocked by treatment with ouabain; in sodium-loaded muscles the ouabain-sensitive fraction of the efflux increases to 75%.2. Under all conditions, the ouabain-insensitive component of the sodium efflux is markedly reduced if the sodium in the external medium is replaced by lithium; at least in sodium-loaded muscles, the ouabain-sensitive component is increased in lithium Ringer.3. Only the ouabain-sensitive component of the efflux is affected by the external potassium concentration.4. In the presence of 2.5 mM-K the sodium influx in a freshly dissected muscle is not significantly altered by ouabain, but in a K-free medium the influx and the efflux are both reduced by nearly 20%.5. The sodium efflux can therefore be regarded as consisting of (1) a sodium-potassium coupled component that is blocked by ouabain and involves a sodium-sodium exchange in the absence of external potassium, and (2) a potassium-insensitive component that is unaffected by ouabain and tends to reach saturation at relatively lower internal sodium concentrations.6. The evidence is considered for attributing component (1) to an efflux of sodium from the sarcoplasm proper, and component (2) to an efflux from the sarcoplasmic reticulum. Although such an interpretation is consistent with many of the observations, a definite identification of the possible sodium compartments in frog muscle cannot yet be made.

Animals↗