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- W2000006723 abstract "Using (3H)etorphine, (3H)E, in binding studies, the KD and Bmax for rabbit mesentery and aorta membrane preparations were 0.61 nM and 0.17 fmol/mg tissue respectively, while it was 0.30 nM and 12 fmol/mg tissue in the brain. The IC50 of dynorphin (1-13) (D1-13) for displacing (3H)E binding in the blood vessel was 20 +/- 2.8 nM (S,E,M,), while PLO17, D-ala2-D-leu5-enkephalin (DADLE) and met5-enkephalin-arg6-phe7 showed very weak inhibition (IC50 greater than 1000nM) though they displaced (3H)E binding very well in the brain. In vitro study showed that D1-13 inhibited electric field stimulation induced vasoconstriction with an IC50 of 53 +/- 12 (rabbit ear artery) and 510 +/- 120 (dog mesenteric artery)nM. Such effect was partially reversed by 1 microM of naloxone. D-ala2-met5-enkephalin and metorphamide displayed much weaker inhibition and DADLE was completely ineffective at doses up to 1 microM. D1-13 did not antagonize noradrenaline (NA) induced vasoconstriction, while phentolamine could abolish vasoconstriction induced either by stimulation or by NA. The result suggests that D1-13 acts presynaptically on neuronal kappa receptor in the blood vessel and inhibits NA release, thus causes vasodilation." @default.
- W2000006723 created "2016-06-24" @default.
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- W2000006723 date "1985-02-01" @default.
- W2000006723 modified "2023-09-23" @default.
- W2000006723 title "Dynorphin receptor in the blood vessel" @default.
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- W2000006723 doi "https://doi.org/10.1016/0143-4179(85)90088-5" @default.
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