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Article: Cannabinoid CB1 receptor and endothelium-dependent hyperpolarization in guinea-pig carotid, rat mesenteric and porcine coronary arteries

TitleCannabinoid CB1 receptor and endothelium-dependent hyperpolarization in guinea-pig carotid, rat mesenteric and porcine coronary arteries
Authors
Issue Date1998
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1998, v. 123 n. 5, p. 968-974 How to Cite?
Abstract1. The purpose of these experiments was to determine whether or not the endothelium-dependent hyperpolarizations of the vascular smooth muscle cells (observed in the presence of inhibitors of nitric oxide synthase and cyclo-oxygenase) can be attributed to the production of an endogenous cannabinoid. 2. Membrane potential was recorded in the guinea-pig carotid, rat mesenteric and porcine coronary arteries by intracellular microelectrodes. 3. In the rat mesenteric artery, the cannabinoid receptor antagonist, SR 141716 (1 μM), did not modify either the resting membrane potential of smooth muscle cells or the endothelium-dependent hyperpolarization induced by acetylcholine (1 μM) (17.3 ± 1.8 mV, n = 4 and 17.8 ± 2.6 mV, n = 4, in control and presence of SR 141716, respectively). Anandamide (30 μM) induced a hyperpolarization of the smooth muscle cells (12.6 ± 1.4 mV, n = 13 and 2.0 ± 3.0 mV, n = 6 in vessels with and without endothelium, respectively) which could not be repeated in the same tissue, whereas acetylcholine was still able to hyperpolarize the preparation. The hyperpolarization induced by anandamide was not significantly influenced by SR 141716 (1 μM). HU-210 (30 μM), a synthetic CB1 receptor agonist, and palmitoylethanolamide (30 μM), a CB2 receptor agonist, did not influence the membrane potential of the vascular smooth muscle cells. 4. In the rat mesenteric artery, the endothelium-dependent hyperpolarizalion induced by acettlcholine (1 μM) (19.0 ± 1.7 mV, n = 6) was not altered by glibenclamide (1 μM; 17.7 ± 2.3 mV, n = 3). However, the combination of charybdotoxin (0.1 μM) plus apamin (0.5 μM) abolished the acetylcholine-induced hyperpolarization and under these conditions, acetylcholine evoked a depolarization (7.7 ± 2.7 mV, n = 3). The hyperpolarization induced by anandamide (30 μM) (12.6 ± 1.4 mV, n = 13) was significantly inhibited by glibenclamide (4.0 ± 0.4 mV, n = 4) but not significantly affected by the charybdotoxin plus apamin (17.3 ± 2.3 mV, n = 4). 5. In the guinea-pig carotid artery, acetylchoiine (1 μM) evoked endothelium-dependent hyperpolarization (18.8 ± 0.7 mV, n = 15). SR 141716 (10 nM to 10 μM), caused a direct, concentration-dependent hyperpolarization (up to 10 mV at 10 μM) and a significant inhibition of the acetylcholine-induced hyperpolarization. Anandamide (0.1 to 3 μM) did not influence the membrane potential. At a concentration of 30 μM, the cannabinoid agonist induced a non-reproducible hyperpolarization (5.6 ± 1.3 mV, n = 10) with a slow onset. SR 141716 (1 μM) did not affect the hyperpolarization induced by 30 μM anandamide (5.3 ± 1.5 mV, n = 3). 6. In the porcine coronary artery, anandamide up to 30 μM did not hyperpolarize or relax the smooth muscle cells. The endothelium-dependent hyperpolarization and relaxation induced by bradykinin were not influenced by SR 141716 (1 μM). 7. These results indicate that the endothelium-dependent hyperpolarizations, observed in the guinea-pig carotid, rat mesenteric and porcine coronary arteries, are not related to the activation of cannabinoid CB1 receptors.
Persistent Identifierhttp://hdl.handle.net/10722/171205
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChataigneau, Ten_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorThollon, Cen_US
dc.contributor.authorVilleneuve, Nen_US
dc.contributor.authorVilaine, JPen_US
dc.contributor.authorDuhault, Jen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:41Z-
dc.date.available2012-10-30T06:12:41Z-
dc.date.issued1998en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1998, v. 123 n. 5, p. 968-974en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171205-
dc.description.abstract1. The purpose of these experiments was to determine whether or not the endothelium-dependent hyperpolarizations of the vascular smooth muscle cells (observed in the presence of inhibitors of nitric oxide synthase and cyclo-oxygenase) can be attributed to the production of an endogenous cannabinoid. 2. Membrane potential was recorded in the guinea-pig carotid, rat mesenteric and porcine coronary arteries by intracellular microelectrodes. 3. In the rat mesenteric artery, the cannabinoid receptor antagonist, SR 141716 (1 μM), did not modify either the resting membrane potential of smooth muscle cells or the endothelium-dependent hyperpolarization induced by acetylcholine (1 μM) (17.3 ± 1.8 mV, n = 4 and 17.8 ± 2.6 mV, n = 4, in control and presence of SR 141716, respectively). Anandamide (30 μM) induced a hyperpolarization of the smooth muscle cells (12.6 ± 1.4 mV, n = 13 and 2.0 ± 3.0 mV, n = 6 in vessels with and without endothelium, respectively) which could not be repeated in the same tissue, whereas acetylcholine was still able to hyperpolarize the preparation. The hyperpolarization induced by anandamide was not significantly influenced by SR 141716 (1 μM). HU-210 (30 μM), a synthetic CB1 receptor agonist, and palmitoylethanolamide (30 μM), a CB2 receptor agonist, did not influence the membrane potential of the vascular smooth muscle cells. 4. In the rat mesenteric artery, the endothelium-dependent hyperpolarizalion induced by acettlcholine (1 μM) (19.0 ± 1.7 mV, n = 6) was not altered by glibenclamide (1 μM; 17.7 ± 2.3 mV, n = 3). However, the combination of charybdotoxin (0.1 μM) plus apamin (0.5 μM) abolished the acetylcholine-induced hyperpolarization and under these conditions, acetylcholine evoked a depolarization (7.7 ± 2.7 mV, n = 3). The hyperpolarization induced by anandamide (30 μM) (12.6 ± 1.4 mV, n = 13) was significantly inhibited by glibenclamide (4.0 ± 0.4 mV, n = 4) but not significantly affected by the charybdotoxin plus apamin (17.3 ± 2.3 mV, n = 4). 5. In the guinea-pig carotid artery, acetylchoiine (1 μM) evoked endothelium-dependent hyperpolarization (18.8 ± 0.7 mV, n = 15). SR 141716 (10 nM to 10 μM), caused a direct, concentration-dependent hyperpolarization (up to 10 mV at 10 μM) and a significant inhibition of the acetylcholine-induced hyperpolarization. Anandamide (0.1 to 3 μM) did not influence the membrane potential. At a concentration of 30 μM, the cannabinoid agonist induced a non-reproducible hyperpolarization (5.6 ± 1.3 mV, n = 10) with a slow onset. SR 141716 (1 μM) did not affect the hyperpolarization induced by 30 μM anandamide (5.3 ± 1.5 mV, n = 3). 6. In the porcine coronary artery, anandamide up to 30 μM did not hyperpolarize or relax the smooth muscle cells. The endothelium-dependent hyperpolarization and relaxation induced by bradykinin were not influenced by SR 141716 (1 μM). 7. These results indicate that the endothelium-dependent hyperpolarizations, observed in the guinea-pig carotid, rat mesenteric and porcine coronary arteries, are not related to the activation of cannabinoid CB1 receptors.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCarotid Arteries - Physiologyen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMesenteric Arteries - Physiologyen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptor, Cannabinoid, Cb2en_US
dc.subject.meshReceptors, Cannabinoiden_US
dc.subject.meshReceptors, Drug - Drug Effects - Physiologyen_US
dc.subject.meshSwineen_US
dc.titleCannabinoid CB1 receptor and endothelium-dependent hyperpolarization in guinea-pig carotid, rat mesenteric and porcine coronary arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0701690en_US
dc.identifier.pmid9535027-
dc.identifier.scopuseid_2-s2.0-0031594723en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031594723&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume123en_US
dc.identifier.issue5en_US
dc.identifier.spage968en_US
dc.identifier.epage974en_US
dc.identifier.isiWOS:000072235600024-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChataigneau, T=6602561430en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridThollon, C=6602540205en_US
dc.identifier.scopusauthoridVilleneuve, N=7003458215en_US
dc.identifier.scopusauthoridVilaine, JP=7004617134en_US
dc.identifier.scopusauthoridDuhault, J=7005108808en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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