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

Altinbas B., Topuz B. B., İLHAN T., YILMAZ M. S., ERDOST H., YALÇIN M.

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, vol.92, no.8, pp.645-654, 2014 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 92 Issue: 8
  • Publication Date: 2014
  • Doi Number: 10.1139/cjpp-2014-0043
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.645-654
  • Keywords: brain arachidonic acid, mean arterial pressure and heart rate, central histaminergic system, microdialysis, cyclooxygenase immunohistochemistry, CRITICAL HEMORRHAGIC HYPOTENSION, PHOSPHOLIPASE A(2) ACTIVATOR, CENTRAL CHOLINERGIC SYSTEM, THROMBOXANE A(2), INDUCED REVERSAL, INJECTED MELITTIN, INVOLVEMENT, RATS, PRESSOR, PHYSIOLOGY
  • Bursa Uludag University Affiliated: Yes


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 mu mol) 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 mu mol) 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 mu mol; 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.