کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5826924 | 1558915 | 2015 | 45 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mechanisms of vasorelaxation induced by the cannabidiol analogue compound O-1602 in the rat small mesenteric artery
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کلمات کلیدی
TRPV1L-nitroarginine methyl ester∆9-THCSKCaAbnormal cannabidiolO-1602KCaVGCCGPCREGTACGRPBKCa - BKC بهDMSO - DMSOIKCa - IKC بهl-NAME - L-NAME∆9-tetrahydrocannabinol - Δ9-تتراهیدروکانیابینولEndothelium - اندوتلیومdimethyl sulphoxide - دی متیل سولفوکسیدVasorelaxation - واکسنtransient receptor potential vanilloid-1 - پتانسیل ترانزیتی vinyloid-1calcitonin gene-related peptide - پپتید مرتبط با ژن کلسی تونینvoltage-gated Ca2+ channels - کانال های Ca2 + دارای ولتاژVoltage-gated potassium channel - کانال پتاسیم با ولتاژcannabinoid receptor - گیرنده های کانابینوئیدG protein-coupled receptor - گیرندههای جفتشونده با پروتئین جی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Mechanisms of vasorelaxation induced by the cannabidiol analogue compound O-1602 in the rat small mesenteric artery Mechanisms of vasorelaxation induced by the cannabidiol analogue compound O-1602 in the rat small mesenteric artery](/preview/png/5826924.png)
چکیده انگلیسی
Atypical cannabinoid O-1602 (5-Methyl-4-[(1R,6R)-3-methyl-6-(1-cyclohexen-1-yl]-1,3-benzenediol) induces vasorelaxation and activates the orphan G protein-coupled receptor GPR55 in human endothelial cells. This study investigates the underlying mechanisms of vasorelaxation induced by this compound. The vasodilator activity was assessed in the rat third order branch of the superior mesenteric artery using a wire myograph. The vasorelaxation was partially endothelium-dependent (pEC50%=5.8±0.3). The endothelial component was antagonized by the putative endothelial receptor antagonists rimonabant (3 µM; pEC50%=5.1±0.2) and O-1918 (10 µM; pEC50%=5.3±0.2) but not by the CB1 and CB2 receptors antagonists AM 251 (10 µM) and AM 630 (10 µM), respectively. The vasorelaxation was not pertussis toxin-sensitive and not mediated through TRPVI receptors or by the release of NO, but was reduced by inhibition of Ca2+ sensitive K+ channels (KCa). In endothelium-denuded vessels, O-1602 abolished CaCl2-induced contraction and the inhibition was apparently reversed by O-1918. O-1602 mediates its vasorelaxant effects partly by an endothelium-dependent pathway involving rimonabant- and O-1918-sensitive targets that are distinct from the classical CB1 and CB2 cannabinoid receptors and might involve activation of KCa. The endothelium-independent relaxation might involve interfering with Ca2+ entry.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 765, 15 October 2015, Pages 107-114
Journal: European Journal of Pharmacology - Volume 765, 15 October 2015, Pages 107-114
نویسندگان
Y.M. Al Suleimani, A.S. Al Mahruqi, C.R. Hiley,