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Article: Nonendothelial aortic source of nitric oxide in Wistar-Kyoto normotensive and spontaneous hypertensive rats.

TitleNonendothelial aortic source of nitric oxide in Wistar-Kyoto normotensive and spontaneous hypertensive rats.
Authors
Issue Date1992
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Biological Signals, 1992, v. 1 n. 6, p. 322-330 How to Cite?
AbstractUsing a recognized inhibitor of nitric oxide (NO) synthesis, Nw-nitro L-arginine methyl ester (L-NAME), we tested the hypothesis of the existence of a nonendothelial source of NO in vascular tissue using rings of rat thoracic aorta in which endothelial cells have been removed by mechanical abrasion and have totally lost their endothelium-dependent relaxation. Contractility of the muscle was tested by recording the concentration-dependent contraction of the preparations induced by an alpha-adrenergic agonist, phenylephrine. Contractility in aortas from Wistar-Kyoto normotensive rats (WKY) and spontaneous hypertensive rats (SHR) was not significantly affected by a 30-min to 2-hour incubation with L-NAME prior to agonist stimulation. However, preparations incubated for 30 min with 1 mM L-arginine (L-ARG) and then washed for 1 h in standard Krebs solution had a significantly reduced contraction to phenylephrine in both WKY and SHR. In these preparations pretreated with L-ARG, L-NAME significantly increased contractility in both WKY and SHR; this effect was prevented by L-ARG but not by D-arginine. Responses to phenylephrine were not inhibited by L-ARG when preparations were incubated from the beginning of the experiment with 1 mM cycloheximide, thus suggesting a dependence on protein synthesis of the attenuation of contraction seen with L-ARG. Intact aortic rings processed for NADPH diaphorase histochemistry, a putative marker for NO synthase, showed NADPH diaphorase reactivity only in the endothelial layer and in the adventitia.(ABSTRACT TRUNCATED AT 250 WORDS)
Persistent Identifierhttp://hdl.handle.net/10722/171571
ISSN

 

DC FieldValueLanguage
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorKitchener, Pen_US
dc.contributor.authorKwan, CYen_US
dc.contributor.authorDaniel, EEen_US
dc.date.accessioned2012-10-30T06:15:44Z-
dc.date.available2012-10-30T06:15:44Z-
dc.date.issued1992en_US
dc.identifier.citationBiological Signals, 1992, v. 1 n. 6, p. 322-330en_US
dc.identifier.issn1016-0922en_US
dc.identifier.urihttp://hdl.handle.net/10722/171571-
dc.description.abstractUsing a recognized inhibitor of nitric oxide (NO) synthesis, Nw-nitro L-arginine methyl ester (L-NAME), we tested the hypothesis of the existence of a nonendothelial source of NO in vascular tissue using rings of rat thoracic aorta in which endothelial cells have been removed by mechanical abrasion and have totally lost their endothelium-dependent relaxation. Contractility of the muscle was tested by recording the concentration-dependent contraction of the preparations induced by an alpha-adrenergic agonist, phenylephrine. Contractility in aortas from Wistar-Kyoto normotensive rats (WKY) and spontaneous hypertensive rats (SHR) was not significantly affected by a 30-min to 2-hour incubation with L-NAME prior to agonist stimulation. However, preparations incubated for 30 min with 1 mM L-arginine (L-ARG) and then washed for 1 h in standard Krebs solution had a significantly reduced contraction to phenylephrine in both WKY and SHR. In these preparations pretreated with L-ARG, L-NAME significantly increased contractility in both WKY and SHR; this effect was prevented by L-ARG but not by D-arginine. Responses to phenylephrine were not inhibited by L-ARG when preparations were incubated from the beginning of the experiment with 1 mM cycloheximide, thus suggesting a dependence on protein synthesis of the attenuation of contraction seen with L-ARG. Intact aortic rings processed for NADPH diaphorase histochemistry, a putative marker for NO synthase, showed NADPH diaphorase reactivity only in the endothelial layer and in the adventitia.(ABSTRACT TRUNCATED AT 250 WORDS)en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_US
dc.relation.ispartofBiological signalsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracic - Drug Effects - Metabolismen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshNadph Dehydrogenase - Metabolismen_US
dc.subject.meshNg-Nitroarginine Methyl Esteren_US
dc.subject.meshNitric Oxide - Metabolism - Secretionen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.titleNonendothelial aortic source of nitric oxide in Wistar-Kyoto normotensive and spontaneous hypertensive rats.en_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1307932-
dc.identifier.scopuseid_2-s2.0-0026952953en_US
dc.identifier.volume1en_US
dc.identifier.issue6en_US
dc.identifier.spage322en_US
dc.identifier.epage330en_US
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridKitchener, P=35549211200en_US
dc.identifier.scopusauthoridKwan, CY=7201421224en_US
dc.identifier.scopusauthoridDaniel, EE=35474017600en_US

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