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Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects.

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  • المؤلفون: Altinbas B;Altinbas B; Topuz BB; İlhan T; Yilmaz MS; Erdost H; Yalcin M
  • المصدر:
    Canadian journal of physiology and pharmacology [Can J Physiol Pharmacol] 2014 Aug; Vol. 92 (8), pp. 645-54. Date of Electronic Publication: 2014 May 27.
  • نوع النشر :
    Journal Article; Research Support, Non-U.S. Gov't
  • اللغة:
    English
  • معلومة اضافية
    • المصدر:
      Publisher: Canadian Science Publishing Country of Publication: Canada NLM ID: 0372712 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1205-7541 (Electronic) Linking ISSN: 00084212 NLM ISO Abbreviation: Can J Physiol Pharmacol Subsets: MEDLINE
    • بيانات النشر:
      Publication: 2011- : Ottawa, ON : Canadian Science Publishing
      Original Publication: Ottawa, National Research Council of Canada.
    • الموضوع:
      Cardiovascular Physiological Phenomena*/drug effects; Arachidonic Acid/*metabolism ; Histamine/*metabolism ; Hypothalamus, Posterior/*metabolism; Animals ; Arachidonic Acid/pharmacology ; Blood Pressure/drug effects ; Chlorpheniramine/pharmacology ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2/metabolism ; Heart Rate/drug effects ; Histamine/pharmacology ; Histamine Antagonists/pharmacology ; Male ; Neurons/drug effects ; Neurons/metabolism ; Neurotransmitter Agents/pharmacology ; Piperidines/pharmacology ; Ranitidine/pharmacology ; Rats, Sprague-Dawley
    • نبذة مختصرة :
      The aim of this study was to explain the involvement of the central histaminergic system in arachidonic acid (AA)-induced cardiovascular effects in normotensive rats using hemodynamic, immunohistochemistry, and microdialysis studies. Intracerebroventricularly (i.c.v.) administered AA (0.25, 0.5, and 1.0 μmol) induced dose- and time-dependent increases in mean arterial pressure and decreased heart rate in conscious normotensive Sprague-Dawley rats. Central injection of AA (0.5 μmol) also increased posterior hypothalamic extracellular histamine levels and produced strong COX-1 but not COX-2 immunoreactivity in the posterior hypothalamus of rats. Moreover, the cardiovascular effects and COX-1 immunoreactivity in the posterior hypothalamus induced by AA (0.5 μmol; i.c.v.) were almost completely blocked by the H2 receptor antagonist ranitidine (50 and 100 nmol; i.c.v.) and partially blocked by the H1 receptor blocker chlorpheniramine (100 nmol; i.c.v.) and the H3-H4 receptor antagonist thioperamide (50 and 100 nmol; i.c.v.). In conclusion, these results indicate that centrally administered AA induces pressor and bradycardic responses in conscious rats. Moreover, we suggest that AA may activate histaminergic neurons and increase extracellular histamine levels, particularly in the posterior hypothalamus. Acting as a neurotransmitter, histamine is potentially involved in AA-induced cardiovascular effects under normotensive conditions.
    • Contributed Indexing:
      Keywords: acide arachidonique cérébral; brain arachidonic acid; central histaminergic system; cyclooxygenase immunohistochemistry; immunohistochimie de la cyclooxygenase; mean arterial pressure and heart rate; microdialyse; microdialysis; pression artérielle moyenne et rythme cardiaque; système histaminergique central
    • الرقم المعرف:
      0 (Histamine Antagonists)
      0 (Neurotransmitter Agents)
      0 (Piperidines)
      27YG812J1I (Arachidonic Acid)
      3U6IO1965U (Chlorpheniramine)
      820484N8I3 (Histamine)
      884KT10YB7 (Ranitidine)
      EC 1.14.99.1 (Cyclooxygenase 1)
      EC 1.14.99.1 (Cyclooxygenase 2)
      II4319BWUI (thioperamide)
    • الموضوع:
      Date Created: 20140729 Date Completed: 20150511 Latest Revision: 20161125
    • الموضوع:
      20250114
    • الرقم المعرف:
      10.1139/cjpp-2014-0043
    • الرقم المعرف:
      25065747