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Article: L-NAME inhibits Mg2+-induced rat aortic relaxation in the absence of endothelium

TitleL-NAME inhibits Mg2+-induced rat aortic relaxation in the absence of endothelium
Authors
KeywordsAorta
Calcium
Endothelium
L-NAME
Magnesium
Nitric oxide
Vascular smooth muscle
Issue Date1999
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, 1999, v. 128 n. 2, p. 493-499 How to Cite?
Abstract1. L-N(G)-nitro-arginine methyl ester (L-NAME; 100 μM), a nitric oxide synthase (NOS) inhibitor, reversed the relaxation induced by 3 μM acetylcholine (ACh) and 2-10 mM Mg2+ in endothelium-intact (+E) rat aortic rings precontracted with 1 μM phenylephrine (PE). In PE-precontracted endothelium-denuded (-E) rat aorta, 3 μM ACh did not, but Mg2+ caused relaxation which was reversed by L-NAME, but not by D-NAME. 2. The concentration response profiles of L-NAME in reversing the equipotent relaxation induced by 5 mM Mg2+ and 0.2 μM ACh were not significantly different. 3. L-NAME (100 μM) also reversed Mg2+-relaxation of -E aorta pre-contracted with 20 mM KCl or 10 μM prostaglandin F(2α) (PGF(2α)). L-N(G)-monomethyl-arginine (L-NMMA; 100 μM) was also effective in reversing the Mg2+-relaxation. 4. Addition of 0.2 mM Ni2+, like Mg2+, caused relaxation of PE-pre-contracted -E aorta, which was subsequently reversed by 100 μM L-NAME. 5. Reversal of the Mg2+-relaxation by 100 μM L-NAME in PE-precontracted -E aorta persisted following pre-incubation with 1 μM dexamethasone or 300 μM aminoguanidine (to inhibit the inducible form of NOS, iNOS). 6. Pretreatment of either +E or -E aortic rings with 100 μM L-NAME caused elevation of contractile responses to Ca2+ in the presence of 1 μM PE. 7. Our results suggest that L-NAME exerts a direct action on, as yet, unidentified vascular smooth muscle plasma membrane protein(s), thus affecting its reactivity to divalent cations leading to the reversal of relaxation. Such an effect of L-NAME is unrelated to the inhibition of endothelial NOS or the inducible NOS.
Persistent Identifierhttp://hdl.handle.net/10722/49301
ISSN
2023 Impact Factor: 6.8
2023 SCImago Journal Rankings: 2.119
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDas, Ren_HK
dc.contributor.authorKravtsov, GMen_HK
dc.contributor.authorBallard, HJen_HK
dc.contributor.authorKwan, CYen_HK
dc.date.accessioned2008-06-12T06:38:53Z-
dc.date.available2008-06-12T06:38:53Z-
dc.date.issued1999en_HK
dc.identifier.citationBritish Journal of Pharmacology, 1999, v. 128 n. 2, p. 493-499en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49301-
dc.description.abstract1. L-N(G)-nitro-arginine methyl ester (L-NAME; 100 μM), a nitric oxide synthase (NOS) inhibitor, reversed the relaxation induced by 3 μM acetylcholine (ACh) and 2-10 mM Mg2+ in endothelium-intact (+E) rat aortic rings precontracted with 1 μM phenylephrine (PE). In PE-precontracted endothelium-denuded (-E) rat aorta, 3 μM ACh did not, but Mg2+ caused relaxation which was reversed by L-NAME, but not by D-NAME. 2. The concentration response profiles of L-NAME in reversing the equipotent relaxation induced by 5 mM Mg2+ and 0.2 μM ACh were not significantly different. 3. L-NAME (100 μM) also reversed Mg2+-relaxation of -E aorta pre-contracted with 20 mM KCl or 10 μM prostaglandin F(2α) (PGF(2α)). L-N(G)-monomethyl-arginine (L-NMMA; 100 μM) was also effective in reversing the Mg2+-relaxation. 4. Addition of 0.2 mM Ni2+, like Mg2+, caused relaxation of PE-pre-contracted -E aorta, which was subsequently reversed by 100 μM L-NAME. 5. Reversal of the Mg2+-relaxation by 100 μM L-NAME in PE-precontracted -E aorta persisted following pre-incubation with 1 μM dexamethasone or 300 μM aminoguanidine (to inhibit the inducible form of NOS, iNOS). 6. Pretreatment of either +E or -E aortic rings with 100 μM L-NAME caused elevation of contractile responses to Ca2+ in the presence of 1 μM PE. 7. Our results suggest that L-NAME exerts a direct action on, as yet, unidentified vascular smooth muscle plasma membrane protein(s), thus affecting its reactivity to divalent cations leading to the reversal of relaxation. Such an effect of L-NAME is unrelated to the inhibition of endothelial NOS or the inducible NOS.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
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_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectAortaen_HK
dc.subjectCalciumen_HK
dc.subjectEndotheliumen_HK
dc.subjectL-NAMEen_HK
dc.subjectMagnesiumen_HK
dc.subjectNitric oxideen_HK
dc.subjectVascular smooth muscleen_HK
dc.titleL-NAME inhibits Mg2+-induced rat aortic relaxation in the absence of endotheliumen_HK
dc.typeArticleen_HK
dc.identifier.emailBallard, HJ: ballard@hkucc.hku.hken_HK
dc.identifier.authorityBallard, HJ=rp00367en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1038/sj.bjp.0702737en_HK
dc.identifier.pmid10510463-
dc.identifier.pmcidPMC1571625en_HK
dc.identifier.scopuseid_2-s2.0-0032861295en_HK
dc.identifier.hkuros53105-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032861295&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume128en_HK
dc.identifier.issue2en_HK
dc.identifier.spage493en_HK
dc.identifier.epage499en_HK
dc.identifier.isiWOS:000082800600030-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridDas, R=7202061890en_HK
dc.identifier.scopusauthoridKravtsov, GM=7003811092en_HK
dc.identifier.scopusauthoridBallard, HJ=7005286310en_HK
dc.identifier.scopusauthoridKwan, CY=7201421224en_HK
dc.identifier.issnl0007-1188-

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