2022-04-192022-04-192008-06Aydın, C. ve Yalçın, M. (2008). "Peripheral mechanisms involved in the pressor and bradycardic effects of centrally administered arachidonic acid". Prostaglandins Leukotrienes and Essential Fatty Acids, 78(6), 361-368.0952-32781532-2823https://doi.org/10.1016/j.plefa.2008.04.007https://www.sciencedirect.com/science/article/pii/S0952327808000549http://hdl.handle.net/11452/25859In 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 mu g 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 mu g 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 mu g; 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 alpha(1) adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10 mu g/kg), a vasopressin V-1 receptor antagonist, or saralasin (250 mu g/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to arachidonic acid (150 mu g; 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.eninfo:eu-repo/semantics/closedAccessSympatho-adrenomedullary outflowCentral cholinergic systemHemorrhaged hypotensive ratsNormotensive conscious ratsThromboxane a2 analogVasopressin secretionInjected u-46619Blood-pressureActivationMelittinBiochemistry & molecular biologyCell biologyEndocrinology & metabolismAdrenergic alpha-antagonistsAngiotensin II type 1 receptor blockersAnimalsArachidonic acidArginine vasopressinBlood pressureCardiovascular systemEpinephrineHeart RateHormone antagonistsInjections, intraventricularMaleNorepinephrinePrazosinRatsRats, sprague-dawleyReninSaralasinVasopressinsArticle0002580223000052-s2.0-4604910018136136878618571395Biochemistry & molecular biologyCell biologyEndocrinology & metabolismHistamine H4 Receptors; Thioperamide; Chlorpheniramine Maleate[Beta mercapto beta,beta cyclopentamethylenepropionyl 2 (o methyltyrosine) 8 arginine] vasopressinAdrenalinArachidonic acidNoradrenalin blood levelPrazosinReninSaralasinVasopressinVasopressin receptor antagonistAdrenalin blood levelAnimal experimentArticleBlood pressure regulationBradycardiaCardiovascular effectClinical evaluationControlled studyDrug effectDHeart rateHormone actionHormone blood levelMaleMean arterial pressureNonhumanNoradrenalin blood levelPlasma renin activityPriority journalProtein blood levelRatSasopressin blood level