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  • 1
    Electronic Resource
    Electronic Resource
    Evidence against prostaglandin-mediation of somatostatin-inhibition of gastric secretions
    Amsterdam : Elsevier
    Regulatory Peptides 10 (1985), S. 259-266 
    Details
    ISSN: 0167-0115
    Keywords: gastric acid secretion ; indomethacin ; pepsin ; prostaglandins ; somatostatin ; stomach
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-0115(85)90020-5
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  • 2
    Electronic Resource
    Electronic Resource
    The effects of nicotine on basal and stimulated gastric secretions in the conscious cat and in isolated guinea pig gastric mucosal cells (1988)
    Springer
    Inflammation research 23 (1988), S. 289-292 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intravenous (i.v.) administration of nicotine in conscious cats significantly stimulated basal gastric acid output. The effect was completely blocked by atropine and ranitidine. Submaximally stimulated gastric acid secretion was not further increased by nicotine. In isolated guinea pig parietal cells nicotine significantly increased basal acid secretion by about 20% and potentiated the response to maximally effective concentrations of histamine but had no influence on the carbachol response. In isolated parietal cells stimulated either by nicotine, histamine or both, atropine pretreatment increased or inhibited the acid response in concentration-dependent manner. From these data, it is concluded that nicotine had direct stimulatory effects on isolated parietal cells and potentiated the histamine mediated response in the isolated cell preparation but not in the intact animal model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02142567
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  • 3
    Electronic Resource
    Electronic Resource
    Are prostaglandins involved in somatostatin mediated inhibition of gastric secretion in the cat? (1986)
    Springer
    Inflammation research 18 (1986), S. 205-209 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of prostaglandins in somatostatin mediated gastric inhibitory effects has been investigated in conscious cats. The effect of somatostatin on pentagastrin-, insulin-and histamine plus bethanechol-stimulated gastric acid and pepsin secretion was determined with and without indomethacin pretreatment. Somatostatin significantly inhibited acid and pepsin secretion and this effect was not diminished by cyclo-oxygenase inhibition. It is concluded that there is no evidence that endogenous prostaglandins mediate the inhibitory effects of somatostatin on gastric acid and pepsin secretion in the cat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01988022
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of burimamide on gastric acid secretion and gastric mucosal blood flow in cats (1973)
    Springer
    Inflammation research 3 (1973), S. 172-172 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965728
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  • 5
    Electronic Resource
    Electronic Resource
    The mechanism whereby growth hormone-release inhibiting hormone (somatostatin) inhibits food stimulated gastric acid secretion in the cat (1975)
    Springer
    Inflammation research 5 (1975), S. 306-310 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Growth hormone-release inhibiting hormone (somatostatin) inhibits the gastric acid response to food in concious cats. We have confirmed that this tetradecapeptide blocks the food stimulated gastrin release. However, the inhibition of gastrin release is delayed relative to that of acid secretion, showing that the inhibition of food stimulated acid secretion is by a primary effect on the acid secretory mechanism. No evidence was found of potentiation of either the gastric acid output or serum concentration of gastric in response to food.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02205235
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  • 6
    Electronic Resource
    Electronic Resource
    Does the gastric mucosa contain inhibitory histamine H1-receptors? (1979)
    Springer
    Inflammation research 9 (1979), S. 76-77 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion From the results it is concluded that in contrast to data reported in the literature, in cats histamine, dimaprit and tolazoline produce an identical acid response and differ only in their affinity to the histamine H2-receptor. The effects of mepyramine and phenoxybenzamine do not indicate the presence of H1-receptors, which is confirmed by missing inhibitory effects of PEA. The effects of the former two, however, suggest that reversal of the histamine dose-response curve is caused by histamine-released catecholamines which are prevented from being released by mepyramine and blocked in their peripheral action by phenoxybenzamine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02024124
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  • 7
    Electronic Resource
    Electronic Resource
    The possible role of histamine-mediated cAMP formation as a link between H2-receptor stimulation and ultrastructural changes in guinea-pig oxyntic cells (1989)
    Springer
    Inflammation research 27 (1989), S. 173-176 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Guinea-pig oxyntic cell tubulin has been isolated andin vitro aggregation has been studied. The spontaneous assembly of isolated tubulin was significantly accelerated and increased bt 1 mmol/l GTP. Histamine and forskolin increased tubulin polymerization only when detergent dispersed oxyntic cells or crude membranes were added. The forskolin response occurred very rapidly with an EC50 of approximately 30 μmol/l and did not require GTP. Histamine promoted tubulin aggregation with an EC50 of about 5 μmol/l only in the presence of GTP. Ranitidine completely inhibited the effects of histamine. From these data it is suggested that, in the oxyntic cell, histamine H2-receptor activated adenylate cyclase and the corresponding increase in cAMP play a role in eliciting characteristic ultrastructural changes by initiating formation of microtubules as a first step in the cascade of events leading to an increase in the secretory surface area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02222231
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  • 8
    Electronic Resource
    Electronic Resource
    The effects of antimitotic and microfilament disrupting agents on functions of isolated guinea-pig parietal cells (1985)
    Springer
    Inflammation research 16 (1985), S. 199-201 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In isolated guinea-pig parietal cells pretreated for 60 min with the H2-antagonist ranitidine, the antimitotic agents colchicine and vinblastine, the microfilament-disrupting agent cytochalasin B resulted in a concentration-dependent inhibition of histamine-stimulated acid secretion up to 80%. Ranitidine reduced histamine binding to the membrane located H2-receptor. The anti-cytoskeletal agents inhibited the cellular histamine uptake but did not effect the histamine methyltransferase activity which was significantly reduced by ranitidine. The data suggest that cytoskeletal elements like microtubules and microfilaments are of very specific functional significance not only in the secretory process of the parietal cell but also for cellular transport mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01983138
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  • 9
    Electronic Resource
    Electronic Resource
    Histidine decarboxylase inhibition byO-methyl-3(+)catechin and gastric acid secretion in the cat (1983)
    Springer
    Inflammation research 13 (1983), S. 249-251 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the conscious cat the histidine decarboxylase inhibitorO-methyl-3(+)catechin (Zy 15029) promoted a dose-dependent atropine-sensitive increase in basal acid output. Gastric acid secretion stimulated by food or insulin at different time intervals after pretreatment with Zy 15029 was dose and time dependently diminished up to 70% whereas acid output following pentagastrin stimulation was not reduced by doses effective against the former two stimuli. Only a high dose, which due to side effects has to be claimed as not tolerable in the cat, reduced acid output by about 40%, when application of Zy 15029 and stimulation were 90 min apart. It is suggested that in the cat gastric acid response following the three different stimuli was at least in part but to a variable extent mediated by endogenous histamine. Dose-dependent side effects of Zy 15029 might have been due to histidine decarboxylase inhibition in brain and changes in histaminergic neutrotransmission.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01967344
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  • 10
    Electronic Resource
    Electronic Resource
    Histamine uptake and metabolism in intact isolated parietal cells (1981)
    Springer
    Inflammation research 11 (1981), S. 223-227 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 3H-Histamine binding, uptake and metabolism were investigated in intact isolated and enriched parietal cells from the dog and guinea pig. Histamine uptake was sodium dependent and followed by intracellular metabolism. The only metabolite that was detected and extracted from cytosol has been identified by TLC to beN r-methylhistamine. The histamineN-methyltransferase activity appeared to be sodium dependent and was inhibited by mepyramine and chlorpromazine, and also by higher concentrations (10−4–10−3 mol/l) of cimetidine. Two blockers of the sodium channel, amiloride and aminoguanidine, also reduced the enzyme activity by an as yet unknown mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01967618
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