scholarly journals Potassium transference in Nitella.

1978 ◽  
Vol 72 (2) ◽  
pp. 203-218 ◽  
Author(s):  
T E Ryan ◽  
C E Barr ◽  
J P Zorn

Transmembrane movements of K+ and Cl- were studied under a variety of experimental conditions. Potassium was found to carry more than 50% of an externally applied inward positive current. The increase in K+ influx was much greater than that predicted by the purely passive model. The increase in Cl- efflux accounted for less than 10% of the applied current, in agreement with the value predicted for passive movement. 2,4-Dinitrophenol (DNP) caused an 80% reduction in K+ transference and a corresponding increase in the measured electrical resistance of the membrane. DNP also reduced the isotopically measured resting K+ influx and caused a substantial increase in both Cl- influx and efflux. Lowering of the pH from 5.7 to 4.7 also reduced the net K+ influx but without drastically altering the membrane resistance. It appears the major portion of an externally applied current does not travel through passive channels, but rather is shunted through a different membrane component. In conjunction with evidence previously establishing the H+ pump as the primary ion pump in Nitella, the data presented here are consistent with a K+/H+ exchange mechanism which can account for the observed net K+ accumulation and maintenance of the membrane potential above the electrochemical equilibrium potential of the major ions. This mechanism appears to be a likely candidate for the current shunt.

1989 ◽  
Vol 54 (1) ◽  
pp. 91-101 ◽  
Author(s):  
Milan Stakić ◽  
Slobodan Milonjić ◽  
Vladeta Pavasović ◽  
Zoja Ilić

Ultrafiltration of three laboratory made silica and two commercial silica sols was studied using Amicon YC membrane in a 200 ml capacity batch-cell. The effect of silica particle size, stirring conditions, pressure, pH and silica contents on ultrafiltration was investigated. The results obtained indicate that the smaller particles have, disregarding the stirring conditions, lower filtration flux. The differences observed in filtration flux are more pronounced in the conditions without stirring. The obtained value of the membrane resistance is independent of the conditions investigated (stirring, pressure, pH, silica contents and particle size). The values of the resistance of polarized solids, specific resistance, and the mass of gel per membrane surface unit were calculated for all experimental conditions.


Potassium chloride is the major salt recycled in most insect excretory systems. Ion and water reabsorption occur in the rectum by active transport of Cl- and largely passive movement of K+. Both these processes are stimulated several fold by a neuropeptide hormone acting via cyclic AMP (cAMP). This Cl- transport process was investigated by using intracellular ion-sensitive microelectrodes, radiotracer flux measurements, voltage clamping, ion substitutions and inhibitors. The mucosal entry step for Cl- is energy-requiring and highly selective, and is stimulated directly by cAMP and luminal K +. Under some experimental conditions, measured electrochemical potentials for cations across the mucosal membrane are too small to drive Cl- entry by NaCl or KC1 cotransport mechanisms; moreover, net 36C1- flux is independent of the apical Na+ potential. Similarly no evidence for a HCO 3 -Cl- exchange was obtained. We conclude that Cl- transport in locust gut is different from mechanisms currently proposed for vertebrate tissues.


1969 ◽  
Vol 53 (4) ◽  
pp. 471-486 ◽  
Author(s):  
T. Hidaka ◽  
H. Kuriyama

Field stimulation of the jejunum elicited successively an action potential of spike form, a slow excitatory depolarization, a slow inhibitory hyperpolarization, and a postinhibitory depolarization as a rebound excitation. The slow depolarization often triggered the spike. The inhibitory potential showed lower threshold than did the excitatory potential. Both the excitatory potentials were abolished by atropine and tetrodotoxin. Effective membrane resistance measured by the intracellular polarizing method was reduced during the peak of the excitatory potential, but the degree of reduction was smaller than that evoked by iontophoretic application of acetylcholine. Conditioning hyperpolarization of the muscle membrane modified the amplitude of the excitatory potential. The estimated reversal potential level for the excitatory potenialt was about 0 mv. No changes could be observed in the amplitude of the inhibitory potential when hyperpolarization was induced with intracellularly applied current. Low [K]o and [Ca]o blocked the generation of the excitatory potential but the amplitude of the inhibitory potential was enhanced in low [K]o. Low [Ca]o and high [Mg]o had no effect on the inhibitory potential.


1996 ◽  
Vol 199 (9) ◽  
pp. 1921-1930
Author(s):  
J A David ◽  
R M Pitman

The effects of activation of a population of [alpha]-bungarotoxin ([alpha]-bgt)-insensitive cholinergic receptors on the soma of the cockroach fast coxal depressor motor neurone (Df) have been examined under two-electrode voltage-clamp conditions. Activation of these receptors was achieved by bath-application either of acetylcholine (ACh) in the presence of [alpha]-bgt or of the muscarinic agonist McN-A-343 (McN). Since these receptors have been shown previously to respond to some nicotinic agonists, we refer to them as 'McN-sensitive or mixed pharmacological profile muscarinic receptors' (mMAChRs). Activation of these receptors normally results in a biphasic response consisting of an initial outward current component, which reverses near -70 mV, and a later (delayed) inwardly directed current, which is only observed at membrane potentials more positive than -40 to -20 mV. The initial outwardly directed component of the McN-induced current appears to result from an increase in K+ conductance since it reverses at potentials close to the K+ equilibrium potential (EK) (approximately -70 mV under the experimental conditions used) and is blocked by internal Cs+. This increase in K+ conductance is probably due to an increase in Ca2+-activated K+ current (IK,Ca) which is known to form a large proportion of the outward current observed when this neurone is depolarized. The delayed inwardly directed current induced by McN results from suppression of a Ca2+ current (ICa) which, in turn, causes a decrease in IK,Ca. The net effect is a reduction in outward current, because IK,Ca is considerably larger than ICa. Evidence for an action of McN upon Ca2+ channels is provided by experiments in which K+ currents have been suppressed by internal Cs+ to reveal inward currents produced by the movement of Ba2+ through voltage-dependent Ca2+ channels. Ba2+ currents observed under these conditions are suppressed by bath application of McN. The inwardly directed current component of the McN response is unlikely to involve direct regulation of IK,Ca, since McN has no effect upon this current when it is induced by brief intracellular Ca2+ injections. Both the initial outwardly directed component and the delayed inwardly directed component of the McN-induced current were suppressed by intracellular injection of the Ca2+ chelator BAPTA. These observations suggest that a rise in [Ca2+]i mediates the electrophysiological effects of McN in Df somata.


1992 ◽  
Vol 262 (3) ◽  
pp. H921-H925 ◽  
Author(s):  
J. M. Anumonwo ◽  
L. C. Freeman ◽  
W. M. Kwok ◽  
R. S. Kass

We have studied delayed rectifier K+ currents (IK) in cells isolated from the sinoatrial node (SAN) region of the guinea pig. Using whole cell patch-clamp procedures, we measured the voltage dependence of IK activation and IK kinetics and the IK equilibrium potential in 4.8 mM extracellular K concentration solutions. Experiments were designed to contrast properties of guinea pig SAN IK with those of IK recorded from SAN cells of the rabbit. We find that guinea pig SAN IK differs from IK recorded from single rabbit SAN cells in its activation threshold, and in the absence of inactivation of whole cell currents recorded over a wide voltage range. These results, along with the relative insensitivity of guinea pig SAN IK to E-4031 and lanthanum, suggest that under our experimental conditions, a strongly rectifying IK component (IK,r) is not the major component of delayed rectification in the guinea pig SAN, as it appears to be in SAN cells of the rabbit.


1986 ◽  
Vol 64 (11) ◽  
pp. 1381-1384 ◽  
Author(s):  
Jean-Pierre Caillé

The intracellular chloride activity (aiCl), measured with Cl-selective microelectrodes on stimulated rabbit papillary muscles (1 Hz) incubated in serum, was 7.2 ± 2.2 mM (48 measurements). Under the same condition, on the quiescent muscle, aiCl was 7.5 ± 2.8 mM (45 measurements). The membrane potential of quiescent papillary muscles and diastolic potential of stimulated papillary muscles were −79.0 ± 0.7 (50 measurements) and −83.5 ± 0.5 mV (50 measurements), respectively. The experimental conditions were chosen to reproduce the in vivo conditions where the Cl equilibrium potential is close to the membrane potential or to the diastolic potential. After correcting for cytoplasmic interference (4 mM) on the aiCl measurements, the Cl equilibrium potential (ECl) was −84 mV. In conclusion, the Cl distribution in cardiac cells bathed in serum is passive as for in vivo cardiac cells.


1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)


1981 ◽  
Vol 78 (6) ◽  
pp. 637-655 ◽  
Author(s):  
H Kuroda ◽  
R Kuroda

Spherical droplets, derived from Physarum plasmodia by incubation in 10 mM caffeine, seemed to be an excellent system for electrophysiological studies because they were large (less than or equal to 300 micrometer in diameter) and because they tolerated intracellular electrodes filled with 3 M KCl and 10 mM EDTA for a few hours. Intact plasmodia, by contrast, gave valid records for only a few minutes. Under standard conditions ([K+]o = 1 mM, [Na+]o = 5 mM, [Ca++]0 = 0.5 mM, [Mg++]o = 2 mM, and [Cl-]o = 6 mM at pH 7.0), the potential difference across droplet membranes was -80 to -120mV, interior negative. The membrane potential was only slightly sensitive to concentration changes for the above-mentioned ions, and was far negative to the equilibrium diffusion potentials calculated from the known internal contents of K, Na, Ca, Mg, and CL (29.4, 1.6, 3.7, 6.5, and 27.8 mmol/kg, respectively). Variations of external pH did have a strong influence on the membrane potential, yielding a slope of 59 mV/pH between pH 6.5 and 5.5. In this pH range, however, the equilibrium potential for H+ (assuming 6.2 less than or equal to pHi less than or equal to 7.0) was greater than 75 mV positive to the observed membrane potential. Membrane potential was directly responsive to metabolic events, being lowered by potassium cyanide, and by cooling from 25 to 12 degrees C. This ensemble of results strongly indicates that the major component of membrane potential in plasmodial droplets of Physarum is generated by an electrogenic ion pump, probably one extruding H+ ions.


1991 ◽  
Vol 261 (5) ◽  
pp. G752-G762 ◽  
Author(s):  
J. R. Crist ◽  
X. D. He ◽  
R. K. Goyal

Intracellular recordings were made from circular smooth muscle cells of the opossum esophagus. Inhibitory junction potentials (IJPs) 8.3 +/- 0.7 mV in amplitude were observed in response to a single pulse (1 ms, 15 mA) of transmural nerve stimulation. Potassium channel blockers apamin (1 microM), tetraethylammonium (10 mM), 4-aminopyridine (250 microM), and cesium chloride (10 mM) did not reduce IJP amplitude. Conditioning hyperpolarizations to the equilibrium potential for potassium were associated with a significant increase in IJP amplitude. A small increase in membrane resistance was observed during the IJP. Changes in external potassium concentration had no significant effect on IJP amplitude acutely. However, prolonged perfusion with potassium-free Krebs solution resulted in a marked decrease in IJP amplitude as did prolonged perfusion with ouabain (0.1 mM). Low-chloride solution (12.4 mM) resulted acutely in an increase in IJP amplitude. Prolonged low-chloride perfusion resulted in a significant decrease in IJP amplitude. The anion exchange chloride channel inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (600 microM) significantly reduced IJP amplitude. These findings suggest that the IJP observed in opossum esophageal circular smooth muscle in response to a single pulse of stimulation is due to a decrease in membrane chloride conductance. The ability of prolonged application of Na-K pump inhibitors to abolish the IJP appears to be due to known secondary effects of these agents in depleting intracellular chloride.


1975 ◽  
Vol 66 (3) ◽  
pp. 269-286 ◽  
Author(s):  
R A Sjodin ◽  
O Ortiz

When frog sartorius muscles recover from Na enrichment in the presence of external K, net K entry into the fibers occurs by both passive movement and active inward transport via a K pump. Under normal conditions, it has not been possible to experimentally distinguish these processes. Fractionation into the flux components must be accomplished from inferences concerning the K conductance or permeability during a period of rapid Na extrusion. The best estimates indicate that 60-80% of the K entry occurs via the K pump. In the presence of Ba ions, the membrane permeability to K is very much reduced. Under these conditions, Na-enriched muscles underwent a normal recovery in the presence of external K, and the amount of inward K movement due to the K pump rose to over 90% of the total K entry. The characteristics of the K pump studied by this means were: (a) essentially complete inhibition by 10(-4) M ouabain, (b) inhibition by [Na]omicron, (c) activation by [K]omicron according to a rectangular hyperbola in the absence of [Na]omicron, (d) linear activation by [Na]iota over a wide range in concentration, (e) zero or undetectably low pumping rate as [Na]iota leads to 0, (f) the number of Na ions actively transported per K ion actively transported is 1.4-1.7 normally and 1.1 in the presence of Ba.


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