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  • HCO3 secretion  (1)
  • Noradrenaline  (1)
  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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    Paper (German National Licenses)
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