Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/22186
Title: Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats
Authors: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.
0000-0002-5600-8162
0000-0001-9496-1475
Yalçın, Murat
Çavun, Sinan
Yılmaz, Mustafa Sertaç
Savcı, Zahide
AAC-9702-2019
AAG-6956-2021
AAH-1571-2021
57192959734
6507468595
8895544100
6603687024
Keywords: Neurosciences & neurology
Posterior hypothalamus
TxA2
Hemorrhagic shock
Cholinergic
Nicotinic
A7nAChR
Restoration
Mecamylamine
Involvement
Prostaglandins
Responses
A(2)
Injected U-46619
Prostanoid receptors
Adrenomedullary outflow
Blood-pressure
Issue Date: 6-Nov-2006
Publisher: Elsevier
Citation: Yalçın, M. vd. (2006). ''Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats''. Brain Research, 1118(1), 43-51.
Abstract: In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood per 100 g body weight over a period of 10 min. Intracerebroventricular (i.c.v.) injection of U-46619 (0.5, 1, 2 mu g) produced a dose- and time-dependent increase in arterial pressure and reversed the hypotension of this condition. Hemorrhage caused small increases in extracellular hypothalamic acetylcholine and choline levels. Intracerebroventricular administration of U-46619 (1 mu g) further increased the levels of extracellular acetylcholine and choline by 57% and 41%, respectively. Pretreatment with SQ29548 (8 pg; i.c.v.), a selective TxA2 receptor antagonist, completely abrogated the effects of subsequent injection of U-46619 (1 mu g; i.c.v.) on arterial pressure and extracellular acetylcholine and choline levels. Pretreatment with mecamylamine (50 pg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, attenuated the pressor effect of U46619 (1 mu g, ix.v.) in hemorrhaged rats whereas pretreatment with atropine (10 mu g; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, had no effect. Interestingly, pretreatment of rats with methyllycaconitine (10 IAg; i.c.v.) or a-bungarotoxin (10 mu g; i.c.v.), selective antagonists of alpha-7 subtype nicotinic acetylcholine receptors (alpha 7nAChRs), partially abolished the pressor effect of U-46619 (1 vg; i.c.v.) in the hypotensive condition. Pretreatment with a combination of mecamylamine plus methyllycaconitine or mecamylamine plus a-bungarotoxin attenuated the reversal effect of U-46619, but only to the same extent as pretreatment with either antagonist alone. In conclusion, i.c.v. administration of U-46619 restores arterial pressure and increases posterior hypothalamic acetylcholine and choline levels by activating central TxA2 receptors in hemorrhaged hypotensive rats. The activation of central nicotinic cholinergic receptors, predominantly alpha 7nAChRs, partially acts as a mediator in the pressor responses to i.c.v. injection of U-46619 under these conditions.
URI: https://doi.org/10.1016/j.brainres.2006.08.014
https://www.sciencedirect.com/science/article/pii/S0006899306023699
http://hdl.handle.net/11452/22186
ISSN: 0006-8993
1872-6240
Appears in Collections:Scopus
Web of Science

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