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  • Domperidone  (2)
  • Haloperidol  (1)
  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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    Paper (German National Licenses)
    Fulltext
  • 3
    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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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