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  • 1985-1989  (4)
Material
Years
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 16 (1985), S. 199-201 
    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
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  • 2
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 18 (1986), S. 205-209 
    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
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  • 4
    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
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