Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/23037
Title: Cardiovascular effect of peripheral injected melittin in normotensive conscious rats: Mediation of the central cholinergic system
Authors: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.
0000-0002-5600-8162
0000-0002-3090-0099
Yalçın, Murat
Aydın, Cenk
Savcı, Vahide
AAG-6956-2021
57192959734
7005426982
6603687024
Keywords: Central cholinergic system
Heart rate
Intraperitoneal
Mean arterial pressure
Melittin
Phospholipase A2
Administered arachidonic-acid
Hemorrhaged hypotensive rats
Thromboxane a2 analog
Blood-pressure
Cdp-choline
Prostanoid receptors
Phospholipase a(2)
Involvement
U-46619
Brain
Biochemistry & molecular biology
Cell biology
Endocrinology & metabolism
Rattus
Issue Date: 2009
Publisher: Elsevier
Citation: Yalçın, M. vd. (2009). "Cardiovascular effect of peripheral injected melittin in normotensive conscious rats: Mediation of the central cholinergic system". Prostaglandins Leukotrienes and Essential Fatty Acids, 81(5-6), 341-347.
Abstract: Recently we demonstrated that centrally administrated melittin, a phospholipase A(2) (PLA(2)) activator, caused the pressor effect in normotensive, conscious rats. In the present study, we aimed to determine the cardiovascular effect of peripherally injected melittin and the involvement of the central cholinergic system on these effects in the normotensive conscious rats. For this reason, 250, 500 or 1000 mu g/kg doses of melittin were injected intraperitoneally to normotensive male Sprague Dawley rats. Melittin produced dose- and time-dependent increases in mean arterial pressure (MAP) and heart rate (HR). Both peripheral (5 mg/kg; i.p.) and central (500 mu g: i.c.v.) pretreatment with indomethacin, nonselective inhibitor of cyclooxygenase (COX) 1 and 2, totally abolished cardiovascular effect of melittin. Intraperitoneal (i.p.) pretreatment with propranolol, a nonselective beta-adrenergic receptor blocker, completely abolished the tachycardic response to melittin. Also, the pressor effect of melittin was partially attenuated in these rats. In order to test the mediation of the central cholinergic system on the pressor and tachycardic effects of melittin, the rats were pretreated with atropine sulfate (10 mu g; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, mecamylamine (50 mu g; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, methyllycaconitine (10 mu g; i.c.v.) or alpha-bungarotoxin (10 mu g; i.c.v.), selective antagonists of alpha 7 subtype nicotinic acetylcholine receptors (alpha 7nAChRs) 15 min prior to melittin (500 mu g/kg; i.p.) injection. Pretreatment with mecamylamine, methyllycaconitine or alpha-bungarotoxin partially diminished the pressor and tachycardic response to melittin in the normotensive conscious rats whereas pretreatment with atropine sulfate had no effect. In conclusion, our data demonstrate that peripherally administered melittin exerts a clear pressor and tachycardic effect by activating COX pathway. The activation of central cholinergic nicotinic receptors, predominantly alpha 7nAChRs, appears to be involved in the pressor and tachycardic effects of the drug.
URI: https://doi.org/10.1016/j.plefa.2009.10.001
https://www.sciencedirect.com/science/article/pii/S0952327809001719
http://hdl.handle.net/11452/23037
ISSN: 0952-3278
Appears in Collections:Scopus
Web of Science

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