Central cannabinoid 1 receptor antagonist administration prevents endotoxic hypotension affecting norepinephrine release in the preoptic anterior hypothalamic area

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dc.contributor.authorVillanueva, Alex A.
dc.contributor.authorMillington, William
dc.contributor.authorCutrera, Rodolfo A.
dc.contributor.authorStouffer, David G.
dc.contributor.authorParsons, Loren H.
dc.contributor.authorCheer, Joseph F.
dc.contributor.authorFeleder, Carlos
dc.contributor.buuauthorYılmaz, Mustafa
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0001-9496-1475tr_TR
dc.contributor.researcheridAAH-1571-2021tr_TR
dc.contributor.scopusid35755102500tr_TR
dc.date.accessioned2021-11-30T08:14:54Z
dc.date.available2021-11-30T08:14:54Z
dc.date.issued2009-12
dc.description.abstractIt is widely assumed that LIPS lowers arterial pressure during sepsis by stimulating release of TNF-alpha and other vasoactive mediators from macrophages. However, recent data from this and other laboratories have shown that LPS hypotension can be prevented by inhibiting afferent impulse flow in the vagus nerve, by blocking neuronal activity in the nucleus of the solitary tract, or by blocking alpha-adrenergic receptors in the preoptic area/anterior hypothalamic area (POA). These findings suggest that the inflammatory signal is conveyed from the periphery to the brain via the vagus nerve, and that endotoxic shock is mediated through a central mechanism that requires activation of POA neurons. In the present study, we tested whether central cannabinoid 1 (CB1) receptors participate in the control of arterial pressure during endotoxemia based on evidence that hypothalamic neurons express CB1 receptors and synthesize the endogenous CB anandamide. We found that intracerebroventricular administration of rimonabant, a CB1 receptor antagonist, inhibited the fall in arterial pressure evoked by LPS significantly in both conscious and anesthetized rats. Rimonabant attenuated both the immediate fall in arterial pressure evoked by LPS and the second, delayed hypotensive phase that leads to tissue ischemia and death. Rimonabant also prevented the associated LPS-induced rise in extracellular fluid norepinephrine concentrations in the POA. Furthermore, rimonabant attenuated the associated increase in plasma TNF-alpha concentrations characteristic of the late phase of endotoxic hypotension. These data indicate that central CB1 receptors may play an important role in the initiation of endotoxic hypotension.tr_TR
dc.description.sponsorshipAlbany College of Pharmacytr_TR
dc.description.sponsorshipAmerican Foundation for Pharmaceutical Educationtr_TR
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Institute on Drug Abuse (NIDA) European Commission (R01DA025890)tr_TR
dc.description.sponsorshipUnited States Department of Health & Human Services National Institutes of Health (NIH) - USA NIH National Institute on Drug Abuse (NIDA) European Commission (R01DA022340)tr_TR
dc.identifier.citationVillanueva, A. vd. (2009). "Central cannabinoid 1 receptor antagonist administration prevents endotoxic hypotension affecting norepinephrine release in the preoptic anterior hypothalamic area". Shock, 32(6), 614-620.tr_TR
dc.identifier.endpage620tr_TR
dc.identifier.issn1073-2322
dc.identifier.issue6tr_TR
dc.identifier.pubmed19295473tr_TR
dc.identifier.scopus2-s2.0-73849115110tr_TR
dc.identifier.startpage614tr_TR
dc.identifier.urihttps://doi.org/10.1097/SHK.0b013e3181a4fd8f
dc.identifier.urihttps://journals.lww.com/shockjournal/Fulltext/2009/12000/CENTRAL_CANNABINOID_1_RECEPTOR_ANTAGONIST.8.aspx
dc.identifier.urihttp://hdl.handle.net/11452/22878
dc.identifier.volume32tr_TR
dc.identifier.wos000272061600008tr_TR
dc.indexed.pubmedPubmedtr_TR
dc.indexed.scopusScopustr_TR
dc.indexed.wosSCIEtr_TR
dc.language.isoentr_TR
dc.publisherLippincott Williams & Wilkinstr_TR
dc.relation.collaborationYurt dışıtr_TR
dc.relation.collaborationSanayitr_TR
dc.relation.journalShocktr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.rightsinfo:eu-repo/semantics/openAccesstr_TR
dc.subjectBlood pressuretr_TR
dc.subjectEndotoxic shocktr_TR
dc.subjectRimonabanttr_TR
dc.subjectSeptic shocktr_TR
dc.subjectTNFtr_TR
dc.subjectFebrile responsetr_TR
dc.subjectVagus nervetr_TR
dc.subjectGuinea-pigstr_TR
dc.subjectAlpha-mshtr_TR
dc.subjectInhibitiontr_TR
dc.subjectRattr_TR
dc.subjectInflammationtr_TR
dc.subjectModulationtr_TR
dc.subjectNeuronstr_TR
dc.subjectLipopolysaccharidetr_TR
dc.subjectGeneral & internal medicinetr_TR
dc.subjectHematologytr_TR
dc.subjectSurgerytr_TR
dc.subjectCardiovascular system & cardiologytr_TR
dc.subject.emtreeCannabinoid 1 receptortr_TR
dc.subject.emtreeCannabinoid 1 receptor antagonisttr_TR
dc.subject.emtreeEndocannabinoidtr_TR
dc.subject.emtreeLipopolysaccharidetr_TR
dc.subject.emtreeNoradrenalintr_TR
dc.subject.emtreeRimonabanttr_TR
dc.subject.emtreeTumor necrosis factor alphatr_TR
dc.subject.emtreeAnimal experimenttr_TR
dc.subject.emtreeAnimal modeltr_TR
dc.subject.emtreeArticletr_TR
dc.subject.emtreeBlood pressuretr_TR
dc.subject.emtreeControlled studytr_TR
dc.subject.emtreeCytokine releasetr_TR
dc.subject.emtreeDose responsetr_TR
dc.subject.emtreeDrug effecttr_TR
dc.subject.emtreeHeart ratetr_TR
dc.subject.emtreeHigh performance liquid chromatographytr_TR
dc.subject.emtreeHypotensiontr_TR
dc.subject.emtreeHypothalamustr_TR
dc.subject.emtreeMaletr_TR
dc.subject.emtreeMass spectrometrytr_TR
dc.subject.emtreeMicrodialysistr_TR
dc.subject.emtreeNeurotransmissiontr_TR
dc.subject.emtreeNonhumantr_TR
dc.subject.emtreeNoradrenalin releasetr_TR
dc.subject.emtreePreoptic areatr_TR
dc.subject.emtreeRattr_TR
dc.subject.emtreeSeptic shocktr_TR
dc.subject.meshAnimalstr_TR
dc.subject.meshAnterior hypothalamic nucleustr_TR
dc.subject.meshArachidonic acidstr_TR
dc.subject.meshBlood pressuretr_TR
dc.subject.meshEndotoxinstr_TR
dc.subject.meshHypotensiontr_TR
dc.subject.meshLipopolysaccharidestr_TR
dc.subject.meshMacrophagestr_TR
dc.subject.meshMaletr_TR
dc.subject.meshNeuronstr_TR
dc.subject.meshNorepinephrinetr_TR
dc.subject.meshPiperidinestr_TR
dc.subject.meshPolyunsaturated alkamidestr_TR
dc.subject.meshPyrazolestr_TR
dc.subject.meshRatstr_TR
dc.subject.meshRats, sprague-dawleytr_TR
dc.subject.meshReceptor, cannabinoid, CB1tr_TR
dc.subject.meshTumor necrosis factor-alphatr_TR
dc.subject.scopusEndocannabinoids; Cannabinoid Receptors; Fatty-Acid Amide Hydrolasetr_TR
dc.subject.wosCritical care medicinetr_TR
dc.subject.wosHematologytr_TR
dc.subject.wosSurgerytr_TR
dc.subject.wosPeripheral vascular diseasetr_TR
dc.titleCentral cannabinoid 1 receptor antagonist administration prevents endotoxic hypotension affecting norepinephrine release in the preoptic anterior hypothalamic areatr_TR
dc.typeArticle
dc.wos.quartileQ1 (Surgery)tr_TR
dc.wos.quartileQ2tr_TR

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