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  • 1
    Electronic Resource
    Electronic Resource
    Stimulation of gallbladder fluid and electrolyte absorption by butyrate (1981)
    Springer
    The journal of membrane biology 62 (1981), S. 183-193 
    Details
    ISSN: 1432-1424
    Keywords: gallbladder ; NaCl absorption ; HCO3 ; short-chain fatty acids ; Na/H-exchange ; HCO3/Cl-Exchange ; active transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Gallbladder fluid and electrolyte transport was investigatedin vitro. In guinea pig gallbladder, equimolar substitution of acetate, propionate, butyrate or valerate for HCO3 was increasingly effective in stimulating fluid absorption. The stimulatory potency of these compounds was a function of their chloroform water partition coefficients. The stimulatory effects of the isomers isobutyrate and isovalerate were less than predicted from their partition coefficients. Acidification of the gallbladder lumen, however, was strictly dependent on the partition coefficients for all of the above fatty acids. Unidirectional22Na fluxes were measured in rabbit and guinea pig gallbladders under short-circuit conditions. In the presence of butyrate stimulation of net Na flux was due entirely to an increase in the mucosal-to-serosal Na flux. Stimulation by butyrate was abolished by its omission from the mucosal bathing solution. The transepithelial electrical potential difference in both rabbit and guinea pig gallbladder became more lumen positive following mucosal but not serosal addition of butyrate. Net14C-butyrate fluxes were too small to account for stimulation of Na absorption in either species. Butyrate stimulation of Na absorption by guinea pig gallbladder was abolished by increasing the bathing pH from 7.4 to 8.1. Tris buffer (25mm) partially inhibited butyrate-dependent gallbladder fluid absorption by rabbit and guinea pig at pH 6.4 and 7.0, respectively, and completely at pH 8.4. These results reveal a marked similarity between butyrate and HCO3 stimulation of gallbladder NaCl and fluid absorption. The results are best explained by a double ion-exchange model, in which butyrate (HCO3) in the mucosal solution acts to maintain the intracellular supply of H+ and butyrate (HCO3) for countertransport of Na and Cl, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01998164
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of bicarbonate on fluid and electrolyte transport by the guinea pig gallbladder: A bicarbonate-chloride exchange (1979)
    Springer
    The journal of membrane biology 45 (1979), S. 43-59 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Fluid transport and net fluxes of Na, K, Cl and HCO3 by guinea pig gallbladder were investigatedin vitro. A perfused gallbladder preparation was devised to simultaneously study unidirectional fluxes of22Na and36Cl. The net Cl flux exceeded the net Na flux during fluid absorption in the presence of HCO3. This Cl excess was counter-balanced by a net HCO3 secretion: a HCO3−Cl exchange. PGE1 reversed the direction of fluid transport and abolished the net Cl flux. The magnitude of the HCO3 secretion remained unchanged, but shifted from a HCO3−Cl exchange to a net secretion of NaHCO3 and KHCO3. Furosemide inhibited both the HCO3−Cl exchange and HCO3 secretion after PGE1 without influencing fluid absorption. Ouabain inhibited the HCO3−Cl exchange as well as fluid absorption; only the effect on the HCO3 secretion was entirely reversible. Secreted HCO3 appeared not to be derived from metabolic sources since HCO3 secretion was abolished in a HCO3-free bathing medium. HCO3 secretion was also dependent on the Na concentration of the bathing fluid. Three lines of evidence are presented in favor of an active HCO3 secretion in guinea pig gallbladder. HCO3 is secreted against: (i) a chemical gradient, (ii) an electrical gradient and (iii) the direction of fluid movement under control conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869294
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of bicarbonate on fluid and electrolyte transport by guinea pig and rabbit gallbladder: Stimulation of absorption (1981)
    Springer
    The journal of membrane biology 62 (1981), S. 175-181 
    Details
    ISSN: 1432-1424
    Keywords: gallbladder ; NaCl absorption ; HCO3 ; Na/H-exchange ; active transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The effect of bicarbonate (HCO3) on fluid absorption by guinea pig gallbladder was investigatedin vitro. Stimulation of fluid absorption was concentration dependent resulting in a fourfold increase in transport over the range 1 to 50mm. Phosphate, Tris, glycodiazine and glutamine buffers failed to substitutte for HCO3 in stimulating absorption. Unidirectional22Na fluxes were measured across short-circuited sheets of guinea pig and rabbit gallbladders mounted in Ussing-type chambers. In both species the net Na flux was unaffected by serosal HCO3 alone but was stimulated by addition of HCO3 to the mucosal bathing solution. Transepithelial electrical potential difference in rabbit gallbladder was about 1.4 mV (lumen positive) when HCO3 was present in the mucosal or in both compartments. This fell to 0.2 mV under HCO3-free conditions or when HCO3 was present only in the serosal solution. The respective values for guinea pig gallbladder were −1.6 and −0.6 mV (lumen negative). HCO3 stimulation of Na absorption by guinea pig gallbladder was abolished by increasing the bathing pH from 7.4 to 7.8, an effect resulting mainly from a reduction inJ mis Na . Tris buffer (25mm) inhibited HCO3-dependent fluid absorption in this species completely at pH 8.5 and partially at 7.5. These results indicate that HCO3 stimulates gallbladder transport in both species by an action from the mucosal side. This effect cannot be attributed to simple buffering of H+ but may be explained by the participation of HCO3 in the maintenance of intracellular H+ for a Na/H-exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01998163
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  • 4
    Electronic Resource
    Electronic Resource
    Selective blockage of cell membrane K conductance by an antisecretory agent in guinea-pig gallbladder epithelium (1989)
    Springer
    Pflügers Archiv 414 (1989), S. 331-339 
    Details
    ISSN: 1432-2013
    Keywords: HCO3 secretion ; Membrane potentials ; Cell membrane ion permeabilities ; Ouabain ; Prostaglandin E1 ; Loperamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Loperamide inhibits PGE1-induced electrogenic HCO3 secretion in guinea-pig gallbladder. Underlying changes in epithelial cell membrane properties were investgated using intracellular microelectrode techniques in vitro. In the absence of PGE1, mucosal loperamide (10−4 mol/l) reversibly depolarized both cell membranes by ∼ 6 mV. The apparent ratio of membrane resistances (R a/R b) remained unchanged and so did voltage responses to luminal Cl removal and Na reduction. The depolarizing response to elevation of luminal K concentration from 5 to 76 mmol/l was decreased from 13 to 8 mV. In the presence of 1 PGE1, the apical membrane is mainly permeable to Cl and HCO3. Under these conditions, loperamide reduced membrane potentials by ∼ 10 mV,R a/R b remaining constant at ∼ 0.4. Effects on voltage responses to changes in luminal Na or K concentration were unchanged. Responses to luminal Cl removal (transient depolarization) were greatly enhanced (from 22 to 42 mV) as predictable from the fall in K permeability that hinders Cl efflux from cell into lumen. Less marked but significant effects were obtained with 10−5 mol/l (mucosal side) and serosal loperamide (10−4 mol/l). We suggest that loperamide inhibits electrogenic HCO3 secretion by reducing apical membrane K permeability. The resulting depolarization diminishes the driving force for conductive anion efflux from cell into lumen. This conclusion is supported by the ability of luminal K elevation to mimick loperamide inhibition of the secretory flux of HCO3 (pH-stat experiments).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584635
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  • 5
    Electronic Resource
    Electronic Resource
    Asymmetric release of cyclic AMP from guinea-pig and rabbit gallbladder (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 358-362 
    Details
    ISSN: 1432-1912
    Keywords: Gallbladder ; Prostaglandins ; cAMP Release ; Fluid secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of cyclic adenosine 3′:5′-monophosphate (cAMP) from guinea-pig and rabbit gallbladder was investigated in vitro. Serosal addition of prostaglandin E1 (PGE1) to luminally perfused guinea-pig gallbladders caused a concentration-dependent efflux of cAMP to the mucosal side, the threshold concentration of PGE1 being 10−7 M. The efflux of cAMP to the serosal side was 7-fold lower. A mucosal sidedness of cAMP release was also observed in stripped preparations of rabbit gallbladder mucosa mounted between two half chambers. No cAMP was found in the solutions bathing the serosal layers isolated from rabbit gallbladders. Fluid secretion was observed at 10−7 M PGE1, an effect mimicked by serosal, but not mucosal application of cAMP (3.3×10−3 M). This is taken to indicate that the basolateral membrane is more easily permeated by cAMP than the apical membrane, since cAMP is believed to exerts its physiological effects from inside the cell. It is concluded that preferential release of cAMP to the mucosal side is not due to a higher permeability of the brush border membrane but rather represents an as yet undefined transport process which may be of importance for the regulation of excessive intracellular cAMP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501178
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  • 6
    Electronic Resource
    Electronic Resource
    Stereospecific inhibition by ozolinone of stimulated chloride secretion in rabbit colon descendens (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 363-367 
    Details
    ISSN: 1432-1912
    Keywords: Rabbit colon ; Chloride secretion ; Diuretics-Ozolinone ; Stereospecific action
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the diuretic drug ozolinone on electrogenic Cl− secretion by rabbit colonic mucosa were investigated in vitro. Electrical properties and unidirectional Cl− fluxes were measured in stripped preparations mounted in Ussing-type chambers. After abolition of electrogenic Na+ absorption by amiloride (10−4 mol/l) on the mucosal side electrogenic Cl− secretion was induced by addition of PGE1 (10−6mol/l, serosal side) and theophylline (10−2mol/l, both sides). Under these conditions, the monitored short-circuit current (Isc) equals the amount of Cl− secreted as evidenced by determination of unidirectional Cl− fluxes. After establishing a stable Cl− secretion its sensitivity to the enantiomers of the diuretic was studied. Only levorotatory (-)-ozolinone, but not the dextrorotatory (+)form, inhibited Cl− secretion on serosal application. This effect was fully accounted for by a reduction in the serosal-to-mucosal Cl− fluxes (J sm Cl ). It was readily reversible and concentration-dependent with a K i value of 6×10−4mol/l, but absent when the drug was added to the mucosal side. The results are in agreement with the hypothesis that loop diuretics inhibit a coupled NaCl entry mechanism across the baso-lateral membrane into colonic epithelial cells. This mechanism is though to account for Cl− influx into the cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501179
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  • 7
    Electronic Resource
    Electronic Resource
    Electrogenic bicarbonate secretion in gallbladder: induction by barium via neuronal, possibly VIP-ergic pathways (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 526-535 
    Details
    ISSN: 1432-1912
    Keywords: Transport regulation ; VIP ; VIP antagonist ; Histamine ; Noradrenaline ; Somatostatin ; Cl− channel blocker ; TMB 8
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In guinea-pig gallbladder epithelium, cAMP converts electroneutral HCO inf3 sup− secretion into an electrogenic process. The effects of blood side Ba2+ (5 mmol/l) on HCO inf3 sup− tranport were investigated in vitro, using pH-stat and voltage clamp techniques to determine unidirectional fluxes of HCO inf3 sup− and transepithelial electrical characteristics. Serosal, not mucosal addition of Ba2+ elevated short-circuit current (Isc), transepithelial potential difference, and tissue conductance; it inhibited the absorptive HCO inf3 sup− flux while leaving the secretory flux unchanged. The Isc effect of Ba2+ was inhibited or prevented by tetrodotoxin; D- and Lrpropranolol; the Cl− channel blocker 4-N-methyl-N-phenylaminothiophene-3-carboxylic acid; the intracellular Ca2+ antagonist, 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester; noradrenaline, by a yohimbine-sensitive action; somatostatin; HCO inf3 sup− -free solutions. Thus Ba2+ appeared to release a neurotransmitter that gives rise to CAMP synthesis sufficcient to turn part of electroneutral HCO inf3 sup− secretion electrogenic. In a search for the involved signalling pathways, the H1-receptor antagonist, cetirizine, largely and hexamethonium, atropine, atenolol, indomethacin, and trifluoperazine entirely failed to antagonize the Isc effect of Ba2+. Similarly, carbachol, dobutamine, salbutamol, and serotonin were unable to mimick the action of Ba2+ and Isc effects of histamine were small and short-lived. By contrast, vasoactive intestinal peptide (VIP; 3 × 10−7 mol/l) completely transformed HCO inf3 sup− secretion into an electrogenic process. The VIP receptor antagonist (4Cl-dPhe6, Leu17)VIP, delayed and reduced the Isc responses to Ba2+ and VIP. As guinea-pig gallbladder epithelial cells possess cAMP-coupled VIP receptors close to VIPergic neurons, Ba2+ is likely to act by releasing VIP from neural terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173214
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of ethacrynic acid on electrolyte and fluid transport by the guinea pig gallbladder (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 309 (1979), S. 287-294 
    Details
    ISSN: 1432-1912
    Keywords: Gallbladder ; Electrolyte transport ; Ethacrynic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of ethacrynic acid on fluid and electrolyte transport by the guinea pig gallbladder was investigated in vitro. 10−4M ethacrynic acid, applied to the serosal side, inhibited fluid and sodium chloride absorption. The reduction in salt absorption was accounted for by a 3 μEq/cm2h decrease in the unidirectional fluxes of Na and Cl from mucosa to serosa with no change in the fluxes from serosa to mucosa. Ethacrynic acid (10−4 M) had no effect on HCO3−Cl exchange, PGE1-induced fluid secretion and inulin permeability. At 10−3 M, ethacrynic acid markedly increased both the serosa to mucosa fluxes of Na and Cl, and the inulin permeability. Examination by light and electron microscopy of gallbladder tissue treated with 10−3 M ethacrynic acid revealed large intracellular vacuoles and occasionally ruptured apical cell membranes. Only slight morphological changes were seen by 10−4 M ethacrynic acid with no changes in the controls and ouabain treated gallbladders. The effects of ethacrynic acid are remarkably different from those of furosemide which has been previously shown to inhibit only the HCO3 secretion leaving fluid and NaCl absorption unchanged.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00504762
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  • 9
    Electronic Resource
    Electronic Resource
    Mechanisms of fluid secretion induced by cAMP and related agents in gallbladder (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 1948-1949 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296127
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  • 10
    Electronic Resource
    Electronic Resource
    Zur Feinstruktur der Neurogliazellen in der Kleinhirnrinde von Säugetieren (1969)
    Springer
    Cell & tissue research 100 (1969), S. 616-633 
    Details
    ISSN: 1432-0878
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Description / Table of Contents: Zusammenfassung Die Kleinhirnrinde von verschiedenen Säugetieren wurde in situ durch Perfusion mit Glutaraldehyd fixiert und licht- und elektronenmikroskopisch untersucht. Die elektronenmikroskopische Analyse zeigt, daß die Fañanas-Zelle eine satellitäre Gliazelle ist, deren Zytoplasmaausläufer keine Gliafilamente enthalten. Das Vorkommen der Fañanas-Zellen beschränkt sich im wesentlichen auf die Purkinjezellschicht; ihre Ausläufer breiten sich nur im unteren Drittel des Stratum moleculare aus. Die Bergmann-Fasern gehören der Astroglia an und zeigen einen entsprechenden submikroskopischen Aufbau mit Bündeln aus Gliafilamenten (Gliafasern) und großem Glykogenreichtum. Die Perikarya der Bergmann-Fasern liegen überwiegend im Stratum granulosum, vereinzelt aber auch in der Purkinje-Zellschicht und im Stratum moleculare. Die Bezeichnung „Golgi-Epithelzelle“ oder „Bergmann-Glia“ muß aufgegeben werden, da die Bergmann-Fasern nicht Ausläufer der satellitären Gliazellen der Purkinje-Zellschicht sind.
    Notes: Summary The cerebellar cortex of different mammalia was fixed with glutaraldehyde in situ by perfusion and investigated with the light- and electron microscope. Special attention is given to the Fañanas cell, Bergmann glia and astrocytes. The electron microscopic study shows that the Fañanas cell represents a pure satellite glial cell. Glial filaments are absent in the cytoplasmic protrusions which extend within the Purkinje cell layer and the lower part of the molecular layer. The Bergmann fibers belong to the astroglia. They exhibit bundles of glial filaments and are rich of glycogen particles. Most of the cell bodies of the Bergmann fibers lie in the Stratum granulosum, some are to be found within the Purkinje cell layer and the molecular layer. The term “Golgi epithelial cell” or “Bergmann glia” should be abandoned because the Bergmann fibers do not belong to the satellite glial cells of the Purkinje cell layer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00344380
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