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Article: L-Arginine evokes both endothelium-dependent and -independent relaxations in L-arginine-depleted aortas of the rat

TitleL-Arginine evokes both endothelium-dependent and -independent relaxations in L-arginine-depleted aortas of the rat
Authors
Issue Date1991
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1991, v. 68 n. 1, p. 209-216 How to Cite?
AbstractThis study was designed to investigate the effects of L-arginine (the substrate for the formation of endothelium-derived nitric oxide) in vascular tissues. Rat aortic rings, with or without endothelium, were suspended in organ chambers for the measurement of isometric tension; they were contracted with phenylephrine (10-6 M). After a short incubation period (0.5 hour) in physiological salt solution, L-arginine induced minor changes in both types of rings. In contrast, when the incubation time was increased (2, 4, 6, and 8 hours), L-arginine evoked concentration- and time-dependent relaxations in aortic rings both with and without endothelium. The relaxations were larger in rings with endothelium. The presence of L-arginine (10-3 M) in the incubation medium inhibited subsequent relaxations evoked by the amino acid. The concentration-relaxation curves associated with acetylcholine in rings with endothelium and the curves associated with Sin-1, a spontaneous donor of nitric oxide, in rings with or without endothelium were slightly but significantly shifted to the right after a 6-hour incubation. Nitro-L-arginine (3 x 10-5 M) and methylene blue (3 x 10-7 M) attenuated the relaxations evoked by L-arginine in rings both with and without endothelium. Other basic amino acids (D-arginine, L-homoarginine, L-citrulline, L-lysine, and L-ornithine; all tested at 10-3 M) either had no effect or induced small relaxations and did not affect the response to L-arginine. These observations suggest that L-arginine specifically and stereoselectively relaxes aortic rings with and without endothelium, probably by restoring the endogenous pool of the amino acid, which is likely depleted by prolonged incubation. Since the relaxations in response to L-arginine are inhibited by nitro-L-arginine in rings both with and without endothelium, the present experiments demonstrate that both the endothelial cells and the vascular smooth muscle possess biochemical pathways converting L-arginine to nitric oxide.
Persistent Identifierhttp://hdl.handle.net/10722/171030
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchini, VBen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:54Z-
dc.date.available2012-10-30T06:11:54Z-
dc.date.issued1991en_US
dc.identifier.citationCirculation Research, 1991, v. 68 n. 1, p. 209-216en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/171030-
dc.description.abstractThis study was designed to investigate the effects of L-arginine (the substrate for the formation of endothelium-derived nitric oxide) in vascular tissues. Rat aortic rings, with or without endothelium, were suspended in organ chambers for the measurement of isometric tension; they were contracted with phenylephrine (10-6 M). After a short incubation period (0.5 hour) in physiological salt solution, L-arginine induced minor changes in both types of rings. In contrast, when the incubation time was increased (2, 4, 6, and 8 hours), L-arginine evoked concentration- and time-dependent relaxations in aortic rings both with and without endothelium. The relaxations were larger in rings with endothelium. The presence of L-arginine (10-3 M) in the incubation medium inhibited subsequent relaxations evoked by the amino acid. The concentration-relaxation curves associated with acetylcholine in rings with endothelium and the curves associated with Sin-1, a spontaneous donor of nitric oxide, in rings with or without endothelium were slightly but significantly shifted to the right after a 6-hour incubation. Nitro-L-arginine (3 x 10-5 M) and methylene blue (3 x 10-7 M) attenuated the relaxations evoked by L-arginine in rings both with and without endothelium. Other basic amino acids (D-arginine, L-homoarginine, L-citrulline, L-lysine, and L-ornithine; all tested at 10-3 M) either had no effect or induced small relaxations and did not affect the response to L-arginine. These observations suggest that L-arginine specifically and stereoselectively relaxes aortic rings with and without endothelium, probably by restoring the endogenous pool of the amino acid, which is likely depleted by prolonged incubation. Since the relaxations in response to L-arginine are inhibited by nitro-L-arginine in rings both with and without endothelium, the present experiments demonstrate that both the endothelial cells and the vascular smooth muscle possess biochemical pathways converting L-arginine to nitric oxide.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAmino Acids - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Metabolismen_US
dc.subject.meshArginine - Deficiency - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolism - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNitric Oxide - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Strainsen_US
dc.subject.meshVasodilationen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleL-Arginine evokes both endothelium-dependent and -independent relaxations in L-arginine-depleted aortas of the raten_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.pmid1984863-
dc.identifier.scopuseid_2-s2.0-0026085330en_US
dc.identifier.volume68en_US
dc.identifier.issue1en_US
dc.identifier.spage209en_US
dc.identifier.epage216en_US
dc.identifier.isiWOS:A1991ER28800021-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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