Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/33068
Title: Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects
Authors: Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı.
0000-0001-9496-1475
0000-0002-5600-8162
Altınbaş, Burçin
Topuz, Bora Burak
İlhan, Tuncay
Yılmaz, Mustafa Sertaç
Erdost, Hatice
Yalçın, Murat
AAH-1571-2021
AAG-6956-2021
AAH-8859-2021
AAH-9216-2021
55356919300
55357889700
16549312600
8895544100
6505787570
57192959734
Keywords: Brain arachidonic acid
Microdialysis
Central histaminergic system
Mean arterial pressure and heart rate
Cyclooxygenase immunohistochemistry
Critical hemorrhagic hypotension
Phospholipase a(2) activator
Pressor
Central cholinergic system
Rats
Thromboxane a(2)
Involvement
Induced reversal
Physiology
Injected melittin
Pharmacology & pharmacy
Physiology
Issue Date: Aug-2014
Publisher: Canadian Science Publishing
Citation: Altınbaş, B. vd. (2014). "Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects". Canadian Journal of Physiology and Pharmacology, 92(8), 645-654.
Abstract: 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.
URI: https://doi.org/10.1139/cjpp-2014-0043
https://cdnsciencepub.com/doi/10.1139/cjpp-2014-0043
http://hdl.handle.net/11452/33068
ISSN: 0008-4212
1205-7541
Appears in Collections:Scopus
Web of Science

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