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  • 1
    Electronic Resource
    Electronic Resource
    Release of Vasoactive Intestinal Peptide in Response to Suckling (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 527 (1988), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1988.tb27026.x
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  • 2
    Electronic Resource
    Electronic Resource
    Bromocriptine and apomorphine stimulation of cortisol secretion in conscious dogs; evidence for a stimulatory site located outside the blood brain barrier (1986)
    Springer
    Psychopharmacology 89 (1986), S. 108-112 
    Details
    ISSN: 1432-2072
    Keywords: Cortisol ; Bromocriptine ; Apomorphine ; Domperidone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract IV injections of the dopamine receptor agonists bromocriptine (0.1 mg/kg) and apomorphine (0.05 mg/kg) induced rapid and long-lasting increases of cortisol levels as measured by RIA in peripheral venous plasma of conscious dogs. Pretreatment with dopamine receptor antagonists which do not readily penetrate the blood brain barrier (domperidone, halopemide, sulpiride) abolished the release responses induced by the dopamine agonists. These results suggest that the dopamine receptor agonists stimulate cortisol release at a site located outside the blood brain barrier. In addition, some dopamine receptor antagonists (haloperidol, chlorpromazine, milenperone) were shown to cause a rapid and long-lasting increase of cortisol levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175200
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of dopamine receptor antagonists on gastrin and vomiting responses to apomorphine (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 16-19 
    Details
    ISSN: 1432-1912
    Keywords: Domperidone ; Halopemide ; Apomorphine ; SCH 23 390 ; Gastrin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Apomorphine (0.05 mg/kg intravenously) was given to conscious dogs, and gastrin levels were measured in peripheral venous blood with a radioimmunoassay. Apomorphine induced an increase of gastrin levels which peaked at 5 min. The peripheral dopamine D-2/DA2 receptor antagonist domperidone (0.2 mg/kg), but not halopemide (0.1–1 mg/kg) nor the D-1 /DA1 receptor antagonist SCH 23390 (0.1 mg/kg), blocked the gastrin response to apomorphine. Both domperidone and halopemide, but not SCH 23 390, blocked the Apomorphine-induced vomiting. These results suggest that apomorphine increases gastrin levels by an action at D-2/DA2 receptors, which are situated outside the blood brain barrier and differ from the receptor inducing the vomiting.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177745
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  • 4
    Electronic Resource
    Electronic Resource
    A long lasting gastrin response to apomorphine revealed by inhibitors of gastric acid secretion (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 20-24 
    Details
    ISSN: 1432-1912
    Keywords: Cimetidine ; Ranitidine ; Omeprazole ; Apomorphine ; Gastrin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Gastrin levels, in the peripheral venous blood of conscious dogs treated with apomorphine (0.05 mg/kg IV), were analysed with a radioimmunoassay. Pretreatment (30 min) with the gastric acid inhibitors cimetidine, ranitidine (H2 receptor antagonists, 4 mg/kg and 1 mg/kg respectively) or omeprazole (H+ − K+ ATPase inhibitor, 1.6 mg/kg) ATPase inhibitor, 1.6 mg/kg prolonged the elevation of gastrin levels occurring in response to an administration of apomorphine. Haloperidol (0.1 mg/kg), but not the peripheral dopamine receptor antagonist domperidone (0.2 mg/kg), abolished the enhanced gastrin response to apomorphine occurring after pretreatment with cimetidine. Cimetidine did not increase the gastrin response to apomorphine in vagotomized dogs. The results are interpreted in terms of an additive gastrin response to apomorphine (different from the short lasting initial peak previously described) which is vagally mediated and inhibited by the gastric acid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00177746
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The benzazepine SCH 23390 increases plasma levels of cortisol in the conscious dog (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 111-112 
    Details
    ISSN: 1432-1912
    Keywords: SCH 23390 ; Haloperidol ; Chlorpromazine ; Plasma levels of cortisol ; Conscious dogs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of neuroleptics on the hypothalamopituitary-adrenal system has been early recognized, but never adequately related to antipsychotic or side effects produced by dopamine antagonists. We are now presenting results showing that the newly characterized dopamine D-1 receptor antagonist, SCH 23390 (0.1 mg/kg i.v.) as well as the mainly dopamine D-2 receptor antagonists, haloperidol (0.1 mg/kg i.v.) and chlorpromazine (1 mg/kg i.v.), produced an increase of cortisol levels (108, 144 and 226% respectively, 20 min after the injection) determined by radioimmunoassay in blood samples collected from superficial veins of the legs of conscious dogs. The 5-HT2 receptor antagonist, cyproheptadine (0.2 mg/kg i.v.), did not modify the cortisol levels. These results suggest that cortisol increase is an effect common to neuroleptic compounds, independently of their relative antagonistic action at dopamine D-1 or D-2 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00633207
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  • 6
    Electronic Resource
    Electronic Resource
    Gastric acid, plasma gastrin, and somatostatin responses to feeding and exogenous gastrin alone and in combination in conscious cats (1987)
    Springer
    Digestive diseases and sciences 32 (1987), S. 177-183 
    Details
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Meat in the stomach or duodenum potentiates pentagastrin-induced acid secretion in cats, presumably by a humoral mechanism. In the present study on cats, a meat meal significantly augmented the maximal acid response from a Heidenhain pouch (HP) to pentagastrin or to human synthetic gastrin I by 31 and 30%, respectively. The maximal HP acid response to pentagastrin was augmented also by peptone instilled into the stomach through a gastric fistula. Intravenous infusion of amino acids stimulated acid secretion but did not augment the maximal acid response to pentagastrin. The plasma concentrations of gastrin and somatostatin increased during infusion of pentagastrin and gastrin I and were not further altered by simultaneous feeding. The present results indicate that the mechanism for potentiation of gastrin-induced acid secretion is of physiological significance, since feeding augmented also the acid response to heptadecapeptide gastrin, the only gastrin secreted from the antrum and duodenum in cats. The potentiation of acid secretion is not dependent on the vagal excitation induced by oral feeding, since potentiation was demonstrated also by intragastric peptone instillation. The mechanism for the potentiation is not due to absorbed amino acids or a decrease of plasma somatostatin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01297106
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