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  • 1
    Electronic Resource
    Electronic Resource
    Arrangement of the subunits of the nicotinic acetylcholine receptor of Torpedo californica as determined by .alpha.-neurotoxin crosslinking (1985)
    s.l. : American Chemical Society
    Biochemistry 24 (1985), S. 2210-2219 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00330a015
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  • 2
    Electronic Resource
    Electronic Resource
    Arginine-specific reagents remove sodium channel inactivation (1978)
    [s.l.] : Nature Publishing Group
    Nature 271 (1978), S. 473-476 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Two methods of internal perfusion were used: the 'roller' method10, and the 'cannula' method11. In either case, axons were then mounted in a plexiglass chamber designed for voltage clamping using conventional techniques"o". Feedback compensation was used in all experiments to reduce errors due to ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/271473a0
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  • 3
    Electronic Resource
    Electronic Resource
    Regulation of the amiloride-blockable sodium channel from epithelial tissue (1990)
    Springer
    Molecular and cellular biochemistry 99 (1990), S. 141-1502 
    Details
    ISSN: 1573-4919
    Keywords: amiloride-sensitive sodium channels ; patch clamp ; protein kinase C2 G proteins ; aldosterone ; epithelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The first step in net active transepithelial transport of sodium in tight epithelia is mediated by the amiloride-blockable sodium channel in the apical membrane. This sodium channel is the primary site for discretionary control of total body sodium and, therefore, investigating its regulatory mechanisms is important to our understanding of the physiology of fluid and electrolyte balance. Because essentially all of the regulatory sites on the channel are on the intracellular surface, patch clamp methods have proven extremely useful in the electrophysiological characterization of the sodium channel by isolating it from other channel proteins in the epithelial membrane and by allowing access to the intracellular surface of the protein. We have examined three different regulatory mechanisms. (1) Inhibition of channel activity by activation of protein kinase C; (2) activation of the channel by agents which activate G-proteins; and (3) modulation of channel kinetics and channel number by mineralocorticoids. Activation of protein kinase C by phorbol esters or synthetic diacylglycerols reduces the open probability of sodium channels. Protein kinase C can be activated in a physiological context by enhancing apical sodium entry. Actions which reduce sodium entry (low luminal sodium concentrations or the apical application of amiloride) increase channel open probability. The link between sodium entry and activation of protein kinase C appears to be mediated by intracellular calcium activity linked to sodium via a sodium/calcium exchange system. Thus, the intracellular sodium concentration is coupled to sodium entry in a negative feedback loop which promotes constant total entry of sodium. Activation of G-proteins by pertussis toxin greatly increases the open probability of sodium channels. Since channels can also be activated by pertussis toxin or GTP gamma S in excised patches, the G-protein appears to be closely linked in the apical membrane to the sodium channel protein itself. The mechanism for activation of this apical G-protein, when most hormonal and transmitter receptors are physically located on the basolateral membrane, is unclear. Mineralocorticoids such as aldosterone have at least two distinct effects. First, as expected, increasing levels of aldosterone increase the density of functional channels detectable in the apical membrane. Second, contrary to expectations, application of aldosterone increases the open probability of sodium channels. Thus aldosterone promotes the functional appearance of new sodium channels and promotes increased sodium entry through both new and pre-existant channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00230344
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  • 4
    Electronic Resource
    Electronic Resource
    Regulation of renal epithelial sodium channels (1992)
    Springer
    Molecular and cellular biochemistry 114 (1992), S. 27-34 
    Details
    ISSN: 1573-4919
    Keywords: amiloride-sensitive sodium channels ; patch-clamp ; vasopressin ; aldosterone ; eicosanoids ; protein kinases
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The high selectivity, low conductance, amiloride-blockable, sodium channel of the mammalian distal nephron (i.e. cortical collecting tubule) is the site of discretionary regulation which allows maintainance of total body sodium balance. In order to understand the physiological events that participate in this regulation, we have used the patch-clamp technique which allows us to measure individual Na+ channel currents and permits access to the cytosolic side of the channel-protein as well as its associated regulatory components. Most of our experiments have utilized the A6 amphibian renal cell line, which when grown on permeable supports is an excellent model for the mammalian distal nephron. Different mechanisms have been examined: (1) regulation by hormonal factors such as Anti-Diuretic Hormone (ADH) and aldosterone, (2) regulation by G-proteins, (3) modulation by protein kinase C (PK-C), and (4) modulation by products of arachidonic acid metabolism. Consistent with noise analysis of tight epithelial tissues, ADH treatment increased the number of active channels in apical membrane patches of A6 cells, without any apparent change in the open probability (Po) of the individual channels. Agents that increased intracellular cAMP mimicked the effects of ADH. In contrast, aldosterone was found to act through a dramatic increase in Po rather than through changes in channel density. Inhibition of methylation by deazaadenosine antagonizes the stimulatory effect of aldosterone. In excised inside-out patches GTPγS inhibits channel activity, whereas GDPβS or pertussis toxin stimulates activity suggesting regulatory control by G-proteins. PK-C has been shown to contribute to ‘feed-back inhibition’ of apical Na+ conductance in tight epithelia. Raising luminal bath sodium and therefore intracellular Na+ inhibits sodium channel activity, an effect that is prevented by PK-C inhibitors and mimicked by PK-C agonists. Cyclooxygenase metabolites of arachidonic acid have an inhibitory effect on channel activity. Finally, a possible role for tyrosine kinase as well as membrane cytoskeleton in the regulation of sodium channel function is also suggested.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00240294
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  • 5
    Electronic Resource
    Electronic Resource
    Acid pH and weak acids induce Na−Cl contransport in the rabbit urinary bladder (1983)
    Springer
    The journal of membrane biology 76 (1983), S. 151-164 
    Details
    ISSN: 1432-1424
    Keywords: rabbit urinary bladder ; tight epithelium ; Na−Cl cotransport ; weak acids ; anion transport ; basolateral membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We have described a coupled Na−Cl entry step at the apical membrane of a tight epithelium, the rabbit urinary bladder. Mucosal pH values, more acid than 4.6, stimulate a 20 to 40-fold increase in mucosal-to-serosal Na+ and Cl− flux. The flux increase is almost completely blocked by low concentrations of bumetanide. The transepithelial movement of Na+ and Cl− is normally electroneutral; however, when weak acids (such as acetate) are present in the mucosal solution, the acid-induced increase in flux is accompanied by a large increase in short-circuit current. Besides blockage by bumetanide, both the increase in flux and short-circuit current are blocked by: (1) Na+-free solutions on the mucosa; (2) Cl−-free solutions on the mucosa; (3) phosphodiesterase inhibitors; (4) ouabain in the serosal solution; (5) K+-free solutions on the serosa; and (6) HCO 3 − -free solutions on the serosa. The increase in the fluxes and the short-circuit current is unaffected by: (1) amiloride application in the mucosal solution; (2) mucosally applied stilbene derivatives which block Cl−/HCO 3 − exchange (SITS); and (3) Cl−-free solutions applied to the serosa. We interpret these results to imply a coupled Na−Cl uptake step at the apical membrane which is stimulated by intracellular acetate (or pH). The uptake step leads to a movement of Na+ and Cl− across the basolateral membrane, which is mediated by the Na+, K+-ATPase and a Na/Cl/HCO 3 − exchange mechanism. Our results demonstrate that “tight” epithelia may, under appropriate circumstances, demonstrate mechanisms of ion movement which are similar to “leaky” epithelia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02000615
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  • 6
    Electronic Resource
    Electronic Resource
    Tetrodotoxin sensitivity of muscle action potentials in pufferfishes and related fishes (1974)
    Springer
    Journal of comparative physiology 89 (1974), S. 59-72 
    Details
    ISSN: 1432-1351
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The effect of tetrodotoxin (TTX) was examined on action potentials in various fishes obtained in the waters of the Great Barrier Reef. The action potentials in muscles of all pufferfishes examined (seven species) were found to be insensitive to 3 × 10−6 M TTX. On the other hand, TTX blocked the action potentials in common hardy-head (Pranesus ogilbyi), slender remora (Echeneis naucrates) and parrotfish (Callyodon pyrrhostethus) at a concentration of 3 × 10−7 M. The dose-response curve fits well the curve predicted by the Langmuir adsorption isotherm. The dissociation constants thus determined in the above mentioned fishes were 3 × 10−8 M, 6 × 10−8 M and 5 × 10−8 M respectively. In contrast to the small dissociation constants found in ordinary fishes, some fishes closely related to pufferfishes have large dissociation constants. They are 3 × 10−7 M in porcupinefish (Diodon holacanthus), 1 × 10−7 M in boxfish (Rhynchostracion nasus) and 5 × 10−7 M in triggerfish (Rhinecanthus aculeatus). We speculate that the resistivity of pufferfish action potentials to TTX is a result of evolutionary change and that the selection may have been done by TTX itself. The effect of saxitoxin (STX) on pufferfish action potentials (Arothron hispidus) was examined and it was found that the action potentials are also resistant to 3 × 10−7 M STX whereas those of common hardy-head (Pranesus ogilbyi) muscle were blocked by 3 × 10−8M. Possible molecular mechanisms of the TTX resistivity are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00696163
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  • 7
    Electronic Resource
    Electronic Resource
    Lipid vesicle-mediated alterations of membrane cholesterol levels: Effects on Na+ and K+ currents in squid axon (1981)
    Springer
    The journal of membrane biology 63 (1981), S. 191-198 
    Details
    ISSN: 1432-1424
    Keywords: Cholesterol exchange ; membrane lipids ; squid axon ; ionic conductances ; flip-flop ; lipid vesicles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary We demonstrate that cholesterol can exchange from sonicated lipid vesicles to a perfused squid giant axon membrane and that vesicles with varying cholesterol/phospholipid (C/P) mole ratios can be used to achieve either net loading or net depletion of axon membrane cholesterol. Two types of evidence were obtained which show that net loading or depletion of cholesterol was achieved: (i) changes in the cholesterol/phospholipid (C/P) mole ratios of axons, and (ii) visualization of cholesterol depleted from the preparation by cholesterol-free vesicles by thin-layer chromatography. The C/P mole ratios indicate that cholesterol levels in the preparation were increased or decreased by 30–40%. Increasing or decreasing membrane cholesterol levels were ineffective in altering the Na+ or K+ occurrents in voltage-clamped axons. In addition, we determined that cholesterol “flip-flop” across the axonal membrane occurred with at 1/2 of 7.3 to 15.3 min.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870980
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  • 8
    Electronic Resource
    Electronic Resource
    Active and passive Na+ fluxes across the basolateral membrane of rabbit urinary bladder (1982)
    Springer
    The journal of membrane biology 67 (1982), S. 219-229 
    Details
    ISSN: 1432-1424
    Keywords: rabbit urinary bladder ; Na+ flux · Na ; K-ATPase ; Na+ transport ; basolateral membrane ; electrogenic transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The apical membrane of rabbit urinary bladder can be functionally removed by application of nystatin at high concentration if the mucosal surface of the tissue is bathed in a saline which mimics intracellular ion concentrations. Under these conditions, the tissue is as far as the movement of univalent ions no more than a sheet of basolateral membrane with some tight junctional membrane in parallel. In this manner the Na+ concentration at the inner surface of the basolateral membrane can be varied by altering the concentration in the mucosal bulk solution. When this was done both mucosal-to-serosal22Na flux and net change in basolateral current were measured. The flux and the current could be further divided into the components of each that were either blocked by ouabain or insensitive to ouabain. Ouabain-insensitive mucosal-to-serosal Na+ flux was a linear function of mucosal Na+ concentration. Ouabain-sensitive Na+ flux and ouabain-sensitive, Na+-induced current both display a saturating relationship which cannot be accounted for by the presence of unstirred layers. If the interaction of Na+ with the basolateral transport process is assumed to involve the interaction of some number of Na+ ions,n, with a maximal flux,M max, then the data can be fit by assuming 3.2 equivalent sites for interaction and a value forM max of 287.8pm cm−2 sec−1 with an intracellular Na concentration of 2.0mm Na+ at half-maximal saturation. By comparing these values with the ouabain-sensitive, Na+-induced current, we calculate a Na+ to K+ coupling ratio of 1.40±0.07 for the transport process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01868663
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  • 9
    Electronic Resource
    Electronic Resource
    Sulfhydryl reagents affect Na+ uptake into toad bladder membrane vesicles (1983)
    Springer
    The journal of membrane biology 71 (1983), S. 39-45 
    Details
    ISSN: 1432-1424
    Keywords: sulfhydryl ; sodium ; amiloride ; toad ; bladder ; vesicle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effect of sulfhydryl reagents on the Na+ permeability mechanisms of toad urinary bladder vesicles was examined. The reagents 5,5′-dithiobis (2-nitrobenzoic acid) (DTNB), iodosobenzoate, and ethylenimine were able to decrease amiloride-inhibited sodium uptake into vesicles when used at low concentrations. When used at higher concentrations these reagents were able to induce large increases in vesicle Na+ permeability that were not sensitive to amiloride. The reagentp-chloro-mercuribenzene sulfonate was able to induce such leaks even at low concentrations. The reagent N-ethylmaleimide was incapable of substantially affecting vesicle Na+ transport in any way. All of the effects observed could be reversed by removing the reagents from the solution surrounding the vesicles. Our results help explain the varied actions of sulfhydryl reagents on intact epithelial tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870673
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  • 10
    Electronic Resource
    Electronic Resource
    The mechanism of Na+ transport by rabbit urinary bladder (1976)
    Springer
    The journal of membrane biology 28 (1976), S. 41-70 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The mechanism of Na+ transport in rabbit urinary bladder has been studied by microelectrode techniques. Of the three layers of epithelium, the apical layer contains virtually all the transepithelial resistance. There is radial cell-to-cell coupling within this layer, but there is no detectable transverse coupling between layers. Cell coupling is apparently interrupted by intracellular injection of depolarizing current. The cell interiors are electrically negative to the bathing solutions, but the apical membrane of the apical layer depolarizes with increasingI sc. Voltage scanning detects no current sinks at the cell junctions or elsewhere. The voltage-divider ratio, α, (ratio of resistance of apical cell membrane,R a, to basolateral cell membrane,R b) decreases from 30 to 0.5 with increasingI sc, because of the transportrelated conductance pathway in the apical membrane. Changes in effective transepithelial capacitance withI sc are predicted and possibly observed. The transepithelial resistance,R t, has been resolved intoR a, Rb, and the junctional resistance,R j, by four different methods: cable analysis, resistance of uncoupled cells, measurements of pairs of (R t, α) values in the same bladder at different transport rates, and the relation betweenR t andI sc and between α andI sc.R j proves to be effectively infinite (nominally 300 kΩ μF) and independent ofI sc, andR a decreases from 154 to 4 kΩ μF with increasingI sc. In the resulting model of Na+ transport in “tight” epithelia, the apical membrane contains an amiloride-inhibited and Ca++-inhibited conductance pathway for Na+ entry; the basolateral membrane contains a Na+−K+-activated ATPase that extrudes Na+; intracellular (Na+) may exert negative feedback on apical membrane conductance; and aldosterone acts to stimulate Na+ entry at the apical membrane via the amiloride-sensitive pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869690
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