Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/28727
Title: Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: The investigation of peripheral mechanisms
Authors: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı.
0000-0002-5600-8162
Yalçın, Murat
Savcı, Vahide
AAG-6956-2021
57192959734
6603687024
Keywords: Brain phospholipase A2 (PLA2)
Animalia
Rattus
Catecholamine
Heart rate (HR)
Hemorrhagic shock
Intracerebroventricular
Mean arterial pressure (MAP)
Melittin
Renin activity
Vasopressin
Sympatho-adrenomedullary outflow
Central cholinergic system
Thromboxane A2 analog
Blood-pressure
Vasopressin secretion
Normotensive rats
Arachidonic-acid
Conscious rats
Cdp-choline
Activation
Issue Date: Dec-2007
Publisher: Churchill Livingstone
Citation: Yalçın, M. ve Savcı, V. (2007). "Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: The investigation of peripheral mechanisms". Neuropeptides, 41(6), 465-475.
Abstract: We have previously shown that centrally injected melittin, a phospholipase A(2) (PLA(2)) activator, increases blood pressure and decreases heart rate in the normotensive conscious rats. In the current study we aimed to determine the cardiovascular effects of melittin in hemorrhaged hypotensive rats and to investigate the mediation of peripheral adrenergic, vasopressinergic and renin angiotensin system in the pressor effect of centrally administrated melittin in both normotensive and hypotensive conditions. Acute hypotensive hemorrhage was performed by withdrawing a total volume of 2.2 ml of blood/100 g body weight over a period of 10 min. Melittin was injected intracerebroventricularly (i.c.v.) at the doses of 1.5 mu g, 3.0 mu g or 6.0 mu g after the stabilization period of hemorrhage procedure. We also repeated previous experiments by injecting melittin (1.5 mu g, 3.0 mu g or 6.0 mu g; i.c.v.) to the normotensive animals. Melittin caused dose- and time-dependent increases in mean arterial pressure (MAP) in normal and hypotensive conditions and decreases in heart rate (HR) in normotensive conscious animals. In hypotensive rats, melittin injected at the dose of 6.0 mu g completely restored the decrease in blood pressure. Plasma adrenaline, noradrenaline, vasopressin levels and renin activity increased after melittin (3.0 mu g; i.c.v) administration in normal conditions. Hemorrhage, itself, produced an increase in these plasma hormone levels and melittin (3.0 mu g; i.c.v.) caused additional increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity in hypotensive conditions. Intravenous pretreatments of rats with prazosin (0.5 mg/kg), an alpha(1), adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10 mu g/kg), a vasopressin V, receptor antagonist, or saralasin (250 mu g/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to melittin (3.0 mu g; i.c.v.) in both normotensive and hypotensive conditions. Besides, the combined administration of these three antagonists before melittin completely abolished the pressor responses to drug in both conditions. Results show that centrally administered melittin, a PLA(2) activator, increases blood pressure and reverses hypotension in hemorrhagic shock. The increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity mediate the pressor responses to melittin in normal and hypotensive conditions.
URI: https://doi.org/10.1016/j.npep.2007.07.002
https://www.sciencedirect.com/science/article/pii/S0143417907000662
http://hdl.handle.net/11452/28727
ISSN: 0143-4179
1532-2785
Appears in Collections:PubMed
Scopus
Web of Science

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