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Article: Endothelium-dependent hyperpolarization in isolated arteries taken from animals treated with NO-synthase inhibitors

TitleEndothelium-dependent hyperpolarization in isolated arteries taken from animals treated with NO-synthase inhibitors
Authors
Issue Date1998
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1998, v. 32 n. 6, p. 944-950 How to Cite?
AbstractTo study the effects of chronic in vivo inhibition of NO synthase on endothelium-dependent hyperpolarization, cell-membrane potential (in individual vascular smooth-muscle cells) and changes in tension (in isolated rings) were recorded from isolated canine coronary arteries and guinea-pig carotid arteries and aortas. In coronary arteries taken from control dogs and contracted with U46619, acetylcholine- and bradykinin-induced endothelium- dependent relaxations, which were unaffected by short-term in vitro exposure to indomethacin but were inhibited partially by L-nitro-arginine (LNA). In coronary arteries taken from dogs treated over the long term in vivo with LNA (30 mg/kg on the first day and 20 mg/kg the 7 following days, i.v.), the response to acetylcholine and bradykinin was inhibited when compared with arteries from control dogs. Short-term in vitro exposure to LNA or indomethacin or both did not influence the effects of either agonist. In these arteries, the hyperpolarizing response to acetylcholine, observed in the presence of LNA and indomethacin, was enhanced, whereas that to bradykinin was partially inhibited. In the guinea pig isolated aorta, the relaxation to bradykinin was abolished by long-term in vivo treatment with L- nitro-arginine-methyl-ester (L-NAME; 1.5 mg/ml, in the drinking water for ≥4 days). In (he isolated guinea pig carotid artery studied in the presence of LNA and indomethacin, acetylcholine induced a hyperpolarization that was not significantly affected by long-term-in vivo treatment with L-NAME. These findings indicate that endothelium-dependent hyperpolarizations are maintained during long-term inhibition of NO synthase and probably act as a back-up mechanism to elicit endothelium-dependent relaxations.
Persistent Identifierhttp://hdl.handle.net/10722/171308
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCorriu, Cen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorPuybasset, Len_US
dc.contributor.authorBea, MLen_US
dc.contributor.authorBerdeaux, Aen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:18Z-
dc.date.available2012-10-30T06:13:18Z-
dc.date.issued1998en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1998, v. 32 n. 6, p. 944-950en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171308-
dc.description.abstractTo study the effects of chronic in vivo inhibition of NO synthase on endothelium-dependent hyperpolarization, cell-membrane potential (in individual vascular smooth-muscle cells) and changes in tension (in isolated rings) were recorded from isolated canine coronary arteries and guinea-pig carotid arteries and aortas. In coronary arteries taken from control dogs and contracted with U46619, acetylcholine- and bradykinin-induced endothelium- dependent relaxations, which were unaffected by short-term in vitro exposure to indomethacin but were inhibited partially by L-nitro-arginine (LNA). In coronary arteries taken from dogs treated over the long term in vivo with LNA (30 mg/kg on the first day and 20 mg/kg the 7 following days, i.v.), the response to acetylcholine and bradykinin was inhibited when compared with arteries from control dogs. Short-term in vitro exposure to LNA or indomethacin or both did not influence the effects of either agonist. In these arteries, the hyperpolarizing response to acetylcholine, observed in the presence of LNA and indomethacin, was enhanced, whereas that to bradykinin was partially inhibited. In the guinea pig isolated aorta, the relaxation to bradykinin was abolished by long-term in vivo treatment with L- nitro-arginine-methyl-ester (L-NAME; 1.5 mg/ml, in the drinking water for ≥4 days). In (he isolated guinea pig carotid artery studied in the presence of LNA and indomethacin, acetylcholine induced a hyperpolarization that was not significantly affected by long-term-in vivo treatment with L-NAME. These findings indicate that endothelium-dependent hyperpolarizations are maintained during long-term inhibition of NO synthase and probably act as a back-up mechanism to elicit endothelium-dependent relaxations.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Drug Effects - Metabolismen_US
dc.subject.meshCarotid Arteriesen_US
dc.subject.meshCoronary Vesselsen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Enzymology - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentialsen_US
dc.subject.meshNitric Oxide - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshSpecies Specificityen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleEndothelium-dependent hyperpolarization in isolated arteries taken from animals treated with NO-synthase inhibitorsen_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.doi10.1097/00005344-199812000-00011en_US
dc.identifier.pmid9869500-
dc.identifier.scopuseid_2-s2.0-0345596366en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0345596366&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue6en_US
dc.identifier.spage944en_US
dc.identifier.epage950en_US
dc.identifier.isiWOS:000077382000011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCorriu, C=6602961498en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridPuybasset, L=7004266282en_US
dc.identifier.scopusauthoridBea, ML=16680985200en_US
dc.identifier.scopusauthoridBerdeaux, A=7005941069en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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