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  • Chloride 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
    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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    Paper (German National Licenses)
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