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  • Gallbladder  (2)
  • active transport  (2)
  • Noradrenaline  (1)
  • 1
    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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  • 2
    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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  • 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
    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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  • 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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