Peripheral mechanisms involved in the pressor and bradycardic effects of centrally administered arachidonic acid
| Autor: | Cenk Aydin, Murat Yalcin |
|---|---|
| Přispěvatelé: | Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı., Aydın, Cenk, Yalçın, Murat, AAG-6956-2021 |
| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Male
Vasopressin Blood pressure regulation Biochemistry & molecular biology Rats sprague-dawley Vasopressin secretion Clinical Biochemistry Plasma renin activity Thromboxane a2 analog chemistry.chemical_compound Norepinephrine Histamine H4 Receptors Thioperamide Chlorpheniramine Maleate Sasopressin blood level Heart Rate Renin Protein blood level Endocrinology & metabolism Priority journal Cardiovascular effect Noradrenalin blood level Receptor antagonist Normotensive conscious rats Adrenalin blood level Mean arterial pressure Cardiovascular system Vasopressin receptor antagonist Arachidonic acid Drug effectD Blood pressure Hemorrhaged hypotensive rats Arginine vasopressin Injections intraventricular Sympatho-adrenomedullary outflow Blood-pressure medicine.drug Adrenergic alpha-antagonists Angiotensin II type 1 receptor blockers medicine.medical_specialty Cell biology Epinephrine medicine.drug_class Vasopressins Central cholinergic system Activation Article Hormone action Internal medicine medicine Prazosin Bradycardia Animals Injected u-46619 Clinical evaluation Animal experiment Antagonist Hormone antagonists Melittin Nonhuman [Beta mercapto beta beta cyclopentamethylenepropionyl 2 (o methyltyrosine) 8 arginine] vasopressin Rats Endocrinology chemistry Rat Adrenalin Saralasin Hormone blood level Controlled study |
| Popis: | In the current study, we aimed to determine the cardiovascular effects of arachidonic acid and peripheral mechanisms mediated these effects in normotensive conscious rats. Studies were performed in male Sprague Dawley rats. Arachidonic acid was injected intracerebroventricularly (i.c.v.) at the doses of 75, 150 or 300 microg and it caused dose- and time-dependent increase in mean arterial pressure and decrease in heart rate in normal conditions. Maximal effects were observed 10 min after 150 and 300 microg dose of arachidonic acid and lasted within 30 min. In order to evaluate the role of main peripheral hormonal mechanisms in those cardiovascular effects, plasma adrenaline, noradrenaline, vasopressin levels and renin activity were measured after arachidonic acid (150 microg; i.c.v.) injection. Centrally injected arachidonic acid increased plasma levels of all these hormones and renin activity. Intravenous pretreatments with prazosin (0.5 mg/kg), an alpha1 adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1, O-Me-Tyr2-Arg8]-vasopressin (10 microg/kg), a vasopressin V1 receptor antagonist, or saralasin (250 microg/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to arachidonic acid (150 microg; i.c.v.) while combined administration of these three antagonists completely abolished the effect. Moreover, both individual and combined antagonist pretreatments fully blocked the bradycardic effect of arachidonic acid. In conclusion, our findings show that centrally administered arachidonic acid increases mean arterial pressure and decreases heart rate in normotensive conscious rats and the increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity appear to mediate the cardiovascular effects of the drug. |
| Databáze: | OpenAIRE |
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