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Anandamide induces endothelium-dependent vasoconstriction and CGRPergic nerve-mediated vasodilatation in the rat mesenteric vascular bed.
J Pharmacol Sci. 2012; 118(4):496-505.JP

Abstract

An endogenous cannabinoid anandamide (N-arachidonoylethanolamide) has been shown to cause vasodilatation in vitro and a brief vasoconstriction followed by prolonged depressor response in vivo. This study investigated the vascular effects of anandamide and underlying mechanisms in rat mesenteric vascular beds. In preparations with an intact endothelium and active tone, anandamide at low concentrations (0.1 - 1 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation, but at high concentrations (10 nM - 1 µM) elicited an initial and sharp increase in perfusion pressure due to vasoconstriction followed by long-lasting vasodilatation in a concentration-dependent manner. Treatment with SR141716A [cannabinoid-1 (CB(1))-receptor antagonist] blunted both the vasoconstrictor and vasodilator responses. Also, removal of the endothelium and indomethacin (cyclooxygenase inhibitor), but not adrenergic denervation with 6-hydoxydopamine (adrenergic neurotoxin), markedly inhibited the vasoconstrictor response to anandamide, while these treatments did not affect vasodilatation. The vasodilatation, but not vasoconstriction, in response to anandamide was markedly attenuated by capsazepine [selective antagonist for transient receptor potential vanilloid-1 (TRPV1)], pretreatment with capsaicin [calcitonin gene-related peptide (CGRP)ergic-nerve depletor], or cold-storage denervation. These results suggest that in rat mesenteric vascular beds, anandamide causes CB(1)-receptor- and prostanoid-mediated endothelium-dependent vasoconstriction and perivascular capsaicin-sensitive CGRPergic nerve-mediated vasodilatation.

Authors+Show Affiliations

Department of Clinical Pharmaceutical Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22510966

Citation

Tamaki, Chihiro, et al. "Anandamide Induces Endothelium-dependent Vasoconstriction and CGRPergic Nerve-mediated Vasodilatation in the Rat Mesenteric Vascular Bed." Journal of Pharmacological Sciences, vol. 118, no. 4, 2012, pp. 496-505.
Tamaki C, Nawa H, Takatori S, et al. Anandamide induces endothelium-dependent vasoconstriction and CGRPergic nerve-mediated vasodilatation in the rat mesenteric vascular bed. J Pharmacol Sci. 2012;118(4):496-505.
Tamaki, C., Nawa, H., Takatori, S., Oda, S., Sendo, T., Zamami, Y., & Kawasaki, H. (2012). Anandamide induces endothelium-dependent vasoconstriction and CGRPergic nerve-mediated vasodilatation in the rat mesenteric vascular bed. Journal of Pharmacological Sciences, 118(4), 496-505.
Tamaki C, et al. Anandamide Induces Endothelium-dependent Vasoconstriction and CGRPergic Nerve-mediated Vasodilatation in the Rat Mesenteric Vascular Bed. J Pharmacol Sci. 2012;118(4):496-505. PubMed PMID: 22510966.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Anandamide induces endothelium-dependent vasoconstriction and CGRPergic nerve-mediated vasodilatation in the rat mesenteric vascular bed. AU - Tamaki,Chihiro, AU - Nawa,Hideki, AU - Takatori,Shingo, AU - Oda,Sakiko, AU - Sendo,Toshiaki, AU - Zamami,Yoshito, AU - Kawasaki,Hiromu, PY - 2012/4/19/entrez PY - 2012/4/19/pubmed PY - 2013/2/5/medline SP - 496 EP - 505 JF - Journal of pharmacological sciences JO - J Pharmacol Sci VL - 118 IS - 4 N2 - An endogenous cannabinoid anandamide (N-arachidonoylethanolamide) has been shown to cause vasodilatation in vitro and a brief vasoconstriction followed by prolonged depressor response in vivo. This study investigated the vascular effects of anandamide and underlying mechanisms in rat mesenteric vascular beds. In preparations with an intact endothelium and active tone, anandamide at low concentrations (0.1 - 1 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation, but at high concentrations (10 nM - 1 µM) elicited an initial and sharp increase in perfusion pressure due to vasoconstriction followed by long-lasting vasodilatation in a concentration-dependent manner. Treatment with SR141716A [cannabinoid-1 (CB(1))-receptor antagonist] blunted both the vasoconstrictor and vasodilator responses. Also, removal of the endothelium and indomethacin (cyclooxygenase inhibitor), but not adrenergic denervation with 6-hydoxydopamine (adrenergic neurotoxin), markedly inhibited the vasoconstrictor response to anandamide, while these treatments did not affect vasodilatation. The vasodilatation, but not vasoconstriction, in response to anandamide was markedly attenuated by capsazepine [selective antagonist for transient receptor potential vanilloid-1 (TRPV1)], pretreatment with capsaicin [calcitonin gene-related peptide (CGRP)ergic-nerve depletor], or cold-storage denervation. These results suggest that in rat mesenteric vascular beds, anandamide causes CB(1)-receptor- and prostanoid-mediated endothelium-dependent vasoconstriction and perivascular capsaicin-sensitive CGRPergic nerve-mediated vasodilatation. SN - 1347-8648 UR - https://www.unboundmedicine.com/medline/citation/22510966/Anandamide_induces_endothelium_dependent_vasoconstriction_and_CGRPergic_nerve_mediated_vasodilatation_in_the_rat_mesenteric_vascular_bed_ L2 - https://linkinghub.elsevier.com/retrieve/pii/JST.JSTAGE/jphs/11236FP DB - PRIME DP - Unbound Medicine ER -