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PubMed1976

Electrical properties and structure of the frog arachnoid membrane.

We have used an in vitro preparation of the frog arachnoid membrane to study the role of this membrane in the maintenance of the "blood-cerebrospinal fluid (csf) barrier". Electron microscopy showed that the membrane was made up of 10-15 layers of flat epithelial cells joined together by numerous cell junctions. The electrical resistance of the preparation was about 2000 ohms cm2. The steady-state transmural potential difference (pd) ranged up to 45 mV, csf positive, and this eliminated by either the addition of ouabain to the csf, or by replacing the NaC1 with TEA C1. The pd across the membrane increased when bicarbonate was added to the external bathing solutions. We conclude that this pd is due to the active transport of sodium from the subural fluid to the csf. In some preparations the transmural pd was reversed, i.e., csf negative, and this was also abolished by the addition of ouabain to the csf, or by replacing chloride with isethionate. We conclude that this pd is related to active chloride transport. These, and other experiments, lead us to the conclusion that the arachnois membrane is involved in the production of the cerebrospinal fluid and the maintenance of the blood-cerebrospinal fluid barrier.

Animals↗
PubMed1991

Contributions of sodium and chloride to ultrastructural damage after dendrotomy.

To determine the contributions of sodium and chloride to ultrastructural changes after mechanical injury, we amputated primary dendrites of cultured mouse spinal neurons in low calcium medium in which sodium chloride had been replaced with either choline chloride or sodium isethionate or sodium propionate. Uninjured cultured neurons were also exposed to the sodium ionophore, monensin. A third set of neurons was injured in medium in which all sodium and calcium chloride had been replaced with sucrose. Neurons injured in low-calcium, low-sodium medium exhibited few ultrastructural changes, except very near the lesion, where there was some dilation of mitochondria and cisternae of the smooth endoplasmic reticulum (SER). Mitochondria in other regions of the neurons developed an electron opaque matrix, and those nearer to the lesion converted to the condensed configuration, characterized by expanded intracristal spaces as well as a dense matrix. If sodium but not chloride was present in the medium, there was some dilation of the Golgi cisternae after injury, as well as some increased electron opacity of the mitochondria. Monensin treated neurons also exhibited dilation of the Golgi cisternae. Neurons injured in sucrose-substituted medium showed none of the changes associated with injury in normal culture medium. These results indicate that sodium influx through the lesion is involved in the dilation of the SER, which is seen even in low-calcium medium, and that a permeant anion, such as chloride, is also involved. This dilation of the SER may result from uptake of calcium released from mitochondria in response to elevated cytosolic sodium. Dilation of the Golgi cisternae appears to be a response only to elevated intracellular sodium. Condensation of the mitochondria after injury is thought to be due to increased demands for ATP synthesis and may involve a "futile cycling" of calcium across the mitochondrial membrane, involving sodium-mediated calcium release in response to elevated intracellular calcium.

Animals↗
PubMed1991

Ca2+ modulates an unspecific cation conductance in olfactory cilia of Xenopus laevis.

Olfactory neurones of Xenopus laevis were studied by the patch clamp technique under voltage-clamp conditions. Isolated receptor cells were obtained by dissociating the olfactory mucosa in a Ca(2+)-free solution. Usually some of the resulting isolated olfactory cells lost all of their cilia during the dissociation procedure. Comparing the currents of cells with cilia to those of cells without cilia, a marked difference was found. When all known voltage-gated currents except the Ca(2+)-current were blocked, cells without cilia showed the voltage-gated Ca(2+)-current alone whereas cells with cilia clearly had an additional conductance gc. It could be activated in two ways, either by Ca2+ entry through Ca(2+)-channels or by Ca2+ entry through the Na/Ca-exchanger working in the reversed mode at positive membrane potentials. This ciliar conductance gc had its reversal potential at 0 mV. Replacing extracellular Cl- by isethionate on the one hand, and Na+ by Cs+ or N-methyl-D-glucamine on the other showed that gc was permeable for cations but not for Cl-. In conclusion, there appears to be a Ca(2+)-dependent unselective cation conductance on the cilia of olfactory neurones. The probable role of gc as the last step an IP3/Ca mediated transduction pathway is suggested.

Animals↗
PubMed1993

Tight-junction tightness of Necturus gall bladder epithelium is not regulated by cAMP or intracellular Ca2+. II. Impedance measurements.

In the preceding publication we have reported that, contrary to the prevailing opinion in the literature, the tight-junction tightness of Necturus gall bladder epithelium is not up-regulated by cAMP-mediated or by Ca(2+)-mediated stimulation. This conclusion was based on our observation that the stimulant-induced increase in transepithelial resistance (Rt) occurred only when the lateral intercellular spaces were allowed to collapse, which suggested that the increase reflected primarily or exclusively the increasing resistance of the lateral spaces (Rlis) rather than the postulated increase in tight-junction resistance (Rj). An alternative explanation could have been that the constancy of Rt after space dilatation reflected an increase Rj that was masked by a concomitant fall in apical and basolateral cell membrane resistances Ra and Rbl. To decide between those possibilities we have performed impedance measurements with transepithelial and intracellular microelectrodes on Necturus gall bladder epithelium. Applying previously developed analysis procedures, the measurements readily showed that elevation of intracellular Ca2+ concentration increased Rlis, but left Rj as well as Ra and Rbl quasi constant. Experiments with forskolin, theophylline or isobutylxanthine, on the other hand, were less clear. These stimulants activated an apical Cl- conductance, which drastically reduced Ra and apparently caused low-frequency polarization effects that could not be accounted for by the classical epithelial equivalent circuit. After elimination of the polarization phenomena by uni- or bilateral substitution of Cl- by isethionate or sulphate, however, we were able to demonstrate that Rj remains constant under cAMP-mediated stimulation irrespective of whether the lateral spaces are kept open or are allowed to collapse. We conclude that the tight-junction resistance of Necturus gall bladder epithelium is not controlled by intracellular Ca2+ or by cAMP-mediated stimulation.

Animals↗
PubMed1982

Further evidence for an inverse relationship between macula densa NaCl concentration and filtration rate.

It has been concluded that tubulo-glomerular feedback mechanism is triggered by changes in NaCl concentration ([NaCl]) at the macula densa. This conclusion is based on the demonstration that changes in filtration rate produced during retrograde perfusion of the loop of Henle depend upon the perfusate [NaCl]. Experiments were performed to evaluate whether the effect on glomerular function of orthograde perfusion of the loop of Henle is consistent with this conclusion. Early proximal flow rate (VEP), stop-flow pressure (PSF), early distal chloride concentration ([C]), and flow rate were measured during perfusion of the loop of Henle with mannitol solution (300 mosm kg-1), 30mM NaCl + mannitol (300 mosm kg-1), 140 mM Na isethionate and artificial tubular fluid. When distal flow exceeded 10 nl min-1, the magnitude of the glomerular response was predictable from the [Cl]. The linear regression line, delta VEP = -0.27 [Cl] + 4.3, did not differ from that obtained previously with the retrograde technique. Retrograde perfusion with 140 mM Na isethionate was without effect on VEP. We conclude that the effect on glomerular function of perfusion of the loop of Henle in either an orthograde or a retrograde direction with these solutions depends upon the chloride concentration at the macula densa.

Animals↗
PubMed1985

Effects of chemical modification of amino groups by two different imidoesters on voltage-clamped nerve fibres of the frog.

Voltage clamped single nerve fibres of the frog Rana esculenta were treated with the amino groups specific reagents ethyl acetimidate and isethionyl acetimidate. Ethyl acetimidate is lipid soluble, relatively non-polar and can penetrate a membrane. Isethionyl acetimidate is lipid-insoluble, polar and membrane-impermeant. Treatment with ethyl acetimidate caused an irreversible reduction of Na currents and a shift of the voltage dependence of the steady-state sodium inactivation, h infinity (E), in the hyperpolarizing direction. The voltage dependence of sodium activation was much less affected and a small shift into the depolarizing direction was observed. By contrast, the non-permeant reagent did not reduce the sodium currents and the shifts of the h infinity (E) curve were smaller than the shifts caused by ethyl acetimidate. Furthermore, a small shift of the voltage-dependence of activation in the hyperpolarizing direction was observed. As the modification procedure with imidoesters does not cause a change of net charge, the results cannot be explained by an effect of surface charge modification; rather, they seem to be due to a direct effect of amino group modification on the voltage dependence of inactivation.

Alkanesulfonates↗
PubMed1976

The influence of chloride on the ouabain-sensitive membrane potential and conductance of crayfish giant axons.

1. Resting potential and current-voltage relation were measured in crayfish giant axons bathed in chloride-free and sodium-free solutions with and without ouabain. 2. Chloride-free solution caused a transient depolarization but did not alter the steady-state membrane potential. Utilizing isethionate as an anion substitute, the membrane resistance increased 12.5%. 3. In the absence of extracellular chloride, ouabain (0.5-1 mM) depolarized the axon 6-7 mV. The shape of the current-voltage relation did not change but the curve was shifted along the current axis. 4. These results indicate that ouabain inhibits a steady-state hyperpolarizing electrogenic pump current of approximately 3 muA/cm2. 5. Extracellular sodium removal from axons equilibrated in chloride-free solutions transiently hyperpolarized the membrane 6-7 mV without a change in membrane resistance. The transient hyperpolarization was ouabain and temperature sensitive. The steady-state potential reached in sodium-free and chloride-free solution was not ouabain sensitive. Temperature sensitivity of the steady-state membrane potential was greatly reduced. 6. The transient hyperpolarization produced by extracellular sodium removal was metabolically driven and may present the expression of a sodium efflux transport current of 7.0-7.5 muA/cm2. 7. Using electrophysiologically measured parameters, sodium and potassium conductance, influx and efflux currents and the coupling ratio for sodium/potassium transport are calculated from a modification of the conductance equation. 8. The sodium/potassium transport coupling ratio for steady-state conditions was estimated at 5:3 (1.67:1).

Animals↗
PubMed1980

The stimulus-secretion coupling of glucose-induced insulin release. XLV. The anion-osmotic hypothesis for exocytosis.

Replacement of extracellular chloride by the impermeant anion isethionate, increase in extracellular osmotic strength by addition of sucrose, or exposure to the anion transport blocking agent probenecid inhibited insulin release evoked by glucose or alpha-ketoisocaproate in rat isolated islets. The inhibition of insulin release due to Cl- substitution was associated with a modest decrease in glucose oxidation, but no significant change in glucose-stimulated 45Ca net uptake by the islets. In the isolated perfused rat pancreas, the isethionate- or sucrose-induced inhibition of insulin release was a rapid and rapidly reversible phenomenon. Chloride substitution by isethionate inhibited more severely the second than the first phase of the secretory response to glucose, and failed to affect the insulin response to gliclazide. A chemosmotic mechanism for exocytosis, as proposed for epinephrine and parathyroid hormone release, may also be involved in insulin release.

Alkanesulfonates↗
PubMed1980

Relationship of transient electrical properties to active sodium transport by toad urinary bladder.

Application of voltage pulses of 10 mV for periods of 9 sec across toad urinary bladder elicits a rapid deflection in transepithelial current. Frequently, the current decays back towards its baseline value during the course of the polarizing pulse. This transient phenomenon can be induced, or its magnitude increased, by raising the mucosal or serosal Na+ concentration. The transient can be abolished by sufficiently hyperpolarizing the tissue (rendering serosa positive to mucosa), by inhibiting transcellular Na+ transport with amiloride or ouabain, and by increasing the serosal K+ concentration. Vasopressin increases net Na+ movement across toad bladder but does not elicit these transients. It is proposed as a working hypothesis for further study that the transient behavior characterized in this study reflects: (1) the partition of Na+ between the apical plasma membrane and contiguous fluid layers, (2) the partition of K+ between the basolateral plasma membrane and adjacent submucosal fluid layer, and (3) the negative feedback interaction between intracellular Na+ activity and Na+ permeability of the apical plasma membrane of the transporting cells.

Amiloride↗
PubMed2005

Isethionate as a product from taurine during nitrogen-limited growth of Klebsiella oxytoca TauN1.

Klebsiella oxytoca TauN1 represents a group of isolates which utilise taurine (2-aminoethanesulfonate) quantitatively as a sole source of combined nitrogen for aerobic growth. During growth, a compound is excreted, which has now been identified as isethionate (2-hydroxyethanesulfonate). An ion-chromatographic separation of isethionate was developed to quantify the putative isethionate, whose identity was confirmed by matrix-assisted, laser-desorption ionisation time-of-flight mass spectrometry. Strain TauN1 utilised taurine (and excreted isethionate) concomitantly with growth. Cell-free extracts contained inducible taurine transaminase, which yielded sulfoacetaldehyde. A soluble, NADP-dependent isethionate dehydrogenase converted sulfoacetaldehyde to isethionate. The enzyme was partially purified and it apparently belonged to the family of short-chain alcohol dehydrogenases.

Acetaldehyde↗
PubMed1986

Peptides increase anion conductance of canine trachea: an effect on tight junctions.

The ionic basis for the rapid reduction in potential difference (dip) produced on luminal addition of substance P and related peptides was analysed by altering the electromotive force and chemical gradients across the isolated, canine tracheal epithelium. The dip could be exaggerated, minimised or reversed by increasing, decreasing or reversing the basal potential difference, and the intercept of the line relating the two was close to zero when the Cl- compositions of the two bathing solutions were identical. Luminal Cl- replacement by a non-permeant anion (isethionate) attenuated the dip which was, however, exaggerated by a permeant anion (nitrate). Replacement of serosal Na+ or luminal HCO3- had no significant effect on the magnitude of the dip. The tachykinins exhibited cross-tachyphylaxis with each other, indicating a common receptor. Bradykinin, a structurally unrelated peptide, also produced dips upon luminal addition, but showed no cross-tachyphylaxis with the tachykinins. Again, a linear relation between basal potential difference and the dip elicited by bradykinin was observed. Based on current awareness of the bioelectric properties of the canine tracheal epithelium, we suggest that these peptides modulate paracellular anion permeabilities.

Animals↗
PubMed1988

Effects of Cl- deficiency on the membrane potential in mouse pancreatic beta-cells.

The membrane potential of mouse pancreatic beta-cells was measured with microelectrodes. In the resting cell (3 mM D-glucose), the membrane potential was -63 +/- 3 mV (mean +/- S.E. for four experiments). In the presence of 3 mM D-glucose, total Cl- substitution by isethionate induced a depolarization by 3-4 mV, and readmission of Cl- induced a hyperpolarization by 3-5 mV. At 10 mM glucose, reduction of Cl- to 12 mM by substituting isethionate for Cl- reversibly shifted the repolarization potential by 6-9 mV in the positive direction and stimulated the burst activity during the initial 2-3 min by increasing the fraction of plateau phase. This was followed by a gradual inhibition of electrical activity, including decrease in fraction of plateau phase and slow wave amplitude. Total substitution of Cl- by isethionate or methyl sulphate reversibly shifted the repolarization potential by 3-4 mV in the positive direction and rapidly inhibited the electrical burst pattern without any initial stimulation. Glucose-induced (10 mM) insulin release (15 min) and 45Ca2+ uptake (3 min) were strongly inhibited by reducing the Cl- concentration to 10 mM (isethionate as substitute) and were further inhibited by further reduction of the Cl- concentration. It is suggested that beta-cells are equipped with on electrogenic Cl- flux, which can affect the burst pattern of electrical activity. The inhibitory effects of Cl- substitution may be explained by an influence of Cl- on the voltage-controlled Ca2+ channels.

Animals↗