Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: The investigation of peripheral mechanisms

Autor: Vahide Savci, Murat Yalcin
Přispěvatelé: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı., Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı., Yalçın, Murat, Savcı, Vahide, AAG-6956-2021
Rok vydání: 2007
Předmět:
Male
Mean arterial pressure (MAP)
Vasopressin
Vasopressin secretion
Hemorrhagic hypotension
Adrenergic
Pressor response
Blood Pressure
Cardiovascular System
Plasma renin activity
Arachidonic-acid
Heart rate (HR)
Rats
Sprague-Dawley
Histamine H4 Receptors
Thioperamide
Chlorpheniramine Maleate
Norepinephrine
chemistry.chemical_compound
Endocrinology
Renin
Renin angiotensin aldosterone system
Endocrinology & metabolism
Priority journal
Normotensive rats
Cardiovascular effect
General Medicine
Mean arterial pressure
Vasopressin receptor antagonist
Blood
Neurology
Hemorrhagic shock
Intracerebroventricular
Catecholamine
lipids (amino acids
peptides
and proteins)
Sympatho-adrenomedullary outflow
Hypotension
Blood-pressure
Thromboxane A2 analog
medicine.drug
Renin activity
medicine.medical_specialty
Epinephrine
Vasopressins
Heart rate
Central cholinergic system
Activation
Hemorrhage
Vasopressin V1 receptor
complex mixtures
Article
Melittin
Cellular and Molecular Neuroscience
Internal medicine
Renin–angiotensin system
Prazosin
medicine
Animalia
Animals
Animal model
Animal experiment
Cdp-choline
Rattus
Endocrine and Autonomic Systems
Neurosciences
Conscious rats
Nonhuman
Melitten
Rats
Noradrenalin
chemistry
Brain phospholipase A2 (PLA2)
Rat
Adrenalin
Saralasin
Controlled study
Zdroj: Neuropeptides. 41:465-475
ISSN: 0143-4179
DOI: 10.1016/j.npep.2007.07.002
Popis: 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 2.2ml of blood/100g body weight over a period of 10min. Melittin was injected intracerebroventricularly (i.c.v.) at the doses of 1.5microg, 3.0microg or 6.0microg after the stabilization period of hemorrhage procedure. We also repeated previous experiments by injecting melittin (1.5microg, 3.0microg or 6.0microg; 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 6.0microg completely restored the decrease in blood pressure. Plasma adrenaline, noradrenaline, vasopressin levels and renin activity increased after melittin (3.0microg; i.c.v) administration in normal conditions. Hemorrhage, itself, produced an increase in these plasma hormone levels and melittin (3.0microg; i.c.v.) caused additional increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity in hypotensive conditions. Intravenous pretreatments of rats with prazosin (0.5mg/kg), an alpha(1) adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10microg/kg), a vasopressin V(1) receptor antagonist, or saralasin (250microg/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to melittin (3.0microg; 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.
Databáze: OpenAIRE
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