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Cherry Professor https://doi.org/10.1017/S0029665113003406 ‘ Endocannabinoids: oynauae at cdmdaos mlctosfrhmnhealth human for implications mediators: acid fatty Polyunsaturated . IPaddress: ypsu :Cnaiod nhmnhealth human in Cannabinoids 3: Symposium n- CPF ntestigo ohahrslrssadmoada reperfusion myocardial and atherosclerosis both of setting the in LC-PUFA 3 (2013), hryL anrgt n iaMichel Lisa and Wainwright* L. 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Foundation Heart British a Studentship by supported was M. L. None. can hypothesis refuted. this or proven before but this, be warranted for are explanation attractive studies an further is bene EC, the the to of linked effects receptors act CB that conjugates the on of preferentially generation the in resulting possibly ua n os leucocytes mouse and human taoaiebt idt CB to eicosapentaenoyl bind both and ethanolamine ethanolamide bene docosahexaenoyl the of some for LC-PUFA oycells tory CPF,i spoal oepoal htthese the that in shift probably a of more consequence probably a are is changes it LC-PUFA, eany taoaiehsbe hw oexert to shown been RAW264 has anti-in ethanolamide hexaenoyl eoeloe htteE r nw oata sites at act to known are CB classical EC the the than other that overlooked be ht ntepeec fhigh of presence the in that, hsatrteblnebtenatvto fCB of activation between balance the alter thus eainhp xs ewe h w nteeefcs The all) effects. means these no in two that by fact the (but suf between some are exist the that relationships there in suggest AMI, least to and at similarities atherosclerosis speaking, of set- Mechanistically setting the CVD. in of effects protective ting demonstrate each 2-AG that and doubt no is There tested. been yet as not although has this receptors, aware CB are we from as distinct far sites at actions the E,dcshxeolehnlmd per ohv a have to af greater appears ethanolamide docosahexaenoyl AEA, eetr nfvu fCB of favour in receptors eicosapentaenoyl compensatory and ethanolamine in by ethanolamide resulting docosahexaenoyl system the lipids, in membrane EC increases of the ance overall of an as activity interpreted be of may this reduction While levels. EC n- https://www.cambridge.org/core LC-PUFA 3 fl maoyefcsi os eioeland peritoneal mouse in effects ammatory ( n- fi · 108 macrophages 7 iyfrCB for nity – CPF in LC-PUFA 3 ) Ccnuae a npr eresponsible be part in may conjugates EC htti ieymasa ellrlvlis level cellular a at means likely this what ; ( 33 ) ned ti luil htthese that plausible is it Indeed, . n- Con . CPF-eie clconjugates acyl LC-PUFA-derived 3 Acknowledgements – https://doi.org/10.1017/S0029665113003406 iaca support Financial Ccnuae a iial exert similarly may conjugates EC fi 2 ilefcsof effects cial Conclusions fl hnfrCB for than n- cso interest of icts 2 ( CPF n h CAEA EC the and LC-PUFA 3 110 fl ‘ . IPaddress: ( 1 surrogate i.3 Fig. ec noeosE levels, EC endogenous uence /CB ) oevr ncnrs to contrast in Moreover, . n- 2 LC-PUFA 3 n- 1 .Hwvr tms not must it However, ). eetr n therefore and receptors ( CPF concen- LC-PUFA 3 108 n CB and 1 170.106.34.90 nhmnin human in , n ’ , 3L-UA since LC-PUFA, -3 109 CB ) 2 2 n docosa- and gnssand agonists , on .L anrgtadL Michel L. and Wainwright L. C. eetr in receptors n – -3/ Cconju- EC 27 Sep2021 at07:50:31 1 fl n amma- 6bal- -6 v. fi fi cient CB cial n- n- 3 3 2 h nomto rmteltrtr o hsreview. this for literature the the gathering drafted to W. from C. contribution information equal an the made authors Both , subjectto theCambridgeCore termsofuse,available at 6 od ,KnoH aaeS Nakane H, Kondo S, Kondo 16. 5 u X sbiK kmt Y Okamoto K, Tsuboi YX, Sun 15. 3 ie R(09 noanbnisadteheart. the H Cadas and A, Fontana V, Marzo Endocannabinoids Di 14. (2009) CR Hiley 13. 2 ete G(07 P5:anwmme ftecanna- the of member new a GPR55: (2007) RG Pertwee 12. DA Andersson J, Petersson PM, Zygmunt 11. 0 aehM uhpdyyP akiS Batkai P, Mukhopadhyay M, Rajesh 10. .DfrN a ,Sutn R Souktani J, Wan N, Defer 9. .NmD,LeM,KmJE Kim MH, Lee DH, Nam 8. .Dl J osR,WyeJ Whyte RA, Ross CJ, Daly 7. J Narayanan AR, Lange D, Gebremedhin 6. .Pce ,Bta uo 20)Cardiovascular (2005) G Kunos & S Batkai P, Pacher 5. 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Med endothelial and atherogenesis, cd n adoaclrdsae ehnssunderlying mechanisms bene disease: cardiovascular and acids fatty polyunsaturated acids. omega-3 of effects cardioprotective 1369 r icltr yfnto nobesity. in dysfunction coron- circulatory with ary associated are levels plasma endocannabinoid 28 eetrbokd nmacrophages. on artery blockade coronary receptor antiin in and system disease endocannabinoid Activated Diabetes eetrpooe ada yfnto,oiaiestress, oxidative dysfunction, in cardiac promotes receptor 1 liver. rat the of ischemia-reperfusion injury in increases 2-arachidonoylglycerol ischemia? cerebral Cell 1159 acute . in after signalling N-acylethanolamines of accumulation ligands. 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T Bisogno G, Carta F, Piscitelli 36. 5 aet ,Ginr ,CraG Carta M, Griinari B, Batetta 35. 4 aaaeS oh aaaiT(03 n-3 (2003) T Hamazaki & M Doshi S, Watanabe 34. , subjectto theCambridgeCore termsofuse,available at auae at cd:terptnilrl nbodpressure blood in role potential their acids: fatty saturated endo- aortic cells. rabbit thelial in production oxide receptor nitric independent cannabinoid CB1/CB2 Anandamide-mediated lo rsuemntrn aaeesi ainswith ambulatory patients and in hypertension. parameters essential supplements mild monitoring pressure acid blood fatty unsaturated er aeadbodpesr naashtzdrats. anaesthetized in pressure Pharmacol blood Arch Schmiedebergs and Naunyn rate in changes heart receptor-mediated CB1 cannabinoid vanilloid and both VR1- induce methanandamide and Anandamide 1823 eaoi ydoe ersetv study. retrospective with a Hypertens patients syndrome: without or hypertriglyceridemic with metabolic and pressure in blood normal-high blood untreated and levels supplementation pressure acids fatty polyunsaturated pressure. blood and eihrlC1cnaiodrcposi haemorrhagic in receptors shock. cannabinoid CB1 peripheral ns mlctsteC1cnaiodrcpo nthe in anandamide. receptor of cannabinoid 278 CB1 action mechanism? the hypotensive the implicates onist understand cannabi- we to responses Pharmacol do pressure blood noids: Triphasic (2012) A receptors. 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Zucker obese in cd ordc coi a n in and fat fatty ectopic (n-3) reduce of to ability acids the mediate may Endocannabinoids Acids mice. 2-arachidonoyl- in brain level reduces glycerol enrichment PUFA n-3 and oynauae at cd(UA de (PUFA) acid fatty Polyunsaturated 279 , – mJPyilHatCr Physiol Circ Heart Physiol J Am Hypertension 1826. 69 fl Nature xestvto ielcigatai md hydro- amide lackingfattyacid mice exsensitivityof – ,51 283. 32 96 165 – hrao x Ther Exp Pharmacol J 8 137 , 14136 , 59. 29 51-7075-8-51. , 390 2073 , 1204 , – 518 , fi 28 144. e epnieest nnaie and anandamide, to responsiveness le, rJNutr J Br – – 682 , Nutr J 14141. 2088. – rsalnisLuo setFatty Essent Leukot Prostaglandins – 1210. 521. – 686. 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