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Article: Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice

TitleAcetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice
Authors
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. 126 n. 1, p. 219-226 How to Cite?
Abstract1. Isometric tension was recorded in isolated rings of aorta, carotid, coronary and mesenteric arteries taken from endothelial nitric oxide synthase knockout mice (eNOS(-/-) mice) and the corresponding wild-type strain (eNOS(+/+) mice). The membrane potential of smooth muscle cells was measured in coronary arteries with intracellular microelectrodes. 2. In the isolated aorta, carotid and coronary arteries from the eNOS(+/+) mice, acetylcholine induced an endothelium-dependent relaxation which was inhibited by N(ω)-L-nitro-arginine. In contrast, in the mesenteric arteries, the inhibition of the cholinergic relaxation required the combination of N(ω)-L-nitro-arginine and indomethacin. 3. The isolated aortal carotid and coronary arteries from the eNOS(-/-) mice did not relax in response to acetylcholine. However, acetylcholine produced an indomethacin-sensitive relaxation in the mesenteric artery from eNOS(-/-) mice. 4. The resting membrane potential of smooth muscle cells from isolated coronary arteries was significantly less negative in the eNOS(-/-) mice (-64.8 ± 1.8 mV, n = 20 and -58.4 ± 1.9 mV, n = 17, for eNOS(+/+) and eNOS(-/-) mice, respectively). In both strains, acetylcholine, bradykinin and substance P did not induce endothelium-dependent hyperpolarizations whereas cromakalim consistently produced hyperpolarizations (-7.9 ± 1.1 mV, n = 8 and -13.8 ± 2.6 mV, n = 4, for eNOS(+/+) and eNOS(-/-) mice, respectively). 5. These findings demonstrate that in the blood vessels studied: (1) in the eNOS(+/+) mice, the endothelium-dependent relaxations to acetylcholine involve either NO or the combination of NO plus a product of cyclo-oxygenase but not EDHF; (2) in the eNOS(-/-) mice, NO-dependent responses and EDHF-like responses were not observed. In the mesenteric arteries acetylcholine releases a cyclo-oxygenase derivative.
Persistent Identifierhttp://hdl.handle.net/10722/171223
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.authorHuang, PLen_US
dc.contributor.authorFishman, MCen_US
dc.contributor.authorDuhault, Jen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:47Z-
dc.date.available2012-10-30T06:12:47Z-
dc.date.issued1999en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1999, v. 126 n. 1, p. 219-226en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171223-
dc.description.abstract1. Isometric tension was recorded in isolated rings of aorta, carotid, coronary and mesenteric arteries taken from endothelial nitric oxide synthase knockout mice (eNOS(-/-) mice) and the corresponding wild-type strain (eNOS(+/+) mice). The membrane potential of smooth muscle cells was measured in coronary arteries with intracellular microelectrodes. 2. In the isolated aorta, carotid and coronary arteries from the eNOS(+/+) mice, acetylcholine induced an endothelium-dependent relaxation which was inhibited by N(ω)-L-nitro-arginine. In contrast, in the mesenteric arteries, the inhibition of the cholinergic relaxation required the combination of N(ω)-L-nitro-arginine and indomethacin. 3. The isolated aortal carotid and coronary arteries from the eNOS(-/-) mice did not relax in response to acetylcholine. However, acetylcholine produced an indomethacin-sensitive relaxation in the mesenteric artery from eNOS(-/-) mice. 4. The resting membrane potential of smooth muscle cells from isolated coronary arteries was significantly less negative in the eNOS(-/-) mice (-64.8 ± 1.8 mV, n = 20 and -58.4 ± 1.9 mV, n = 17, for eNOS(+/+) and eNOS(-/-) mice, respectively). In both strains, acetylcholine, bradykinin and substance P did not induce endothelium-dependent hyperpolarizations whereas cromakalim consistently produced hyperpolarizations (-7.9 ± 1.1 mV, n = 8 and -13.8 ± 2.6 mV, n = 4, for eNOS(+/+) and eNOS(-/-) mice, respectively). 5. These findings demonstrate that in the blood vessels studied: (1) in the eNOS(+/+) mice, the endothelium-dependent relaxations to acetylcholine involve either NO or the combination of NO plus a product of cyclo-oxygenase but not EDHF; (2) in the eNOS(-/-) mice, NO-dependent responses and EDHF-like responses were not observed. In the mesenteric arteries acetylcholine releases a cyclo-oxygenase derivative.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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Physiologyen_US
dc.subject.meshBlood Vessels - Drug Effects - Physiologyen_US
dc.subject.meshCarotid Arteries - Drug Effects - Physiologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshCromakalim - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshHomozygoteen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMesenteric Arteries - Drug Effects - Physiologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMolsidomine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshMutationen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitors - Geneticsen_US
dc.subject.meshNitric Oxide Synthase Type Iien_US
dc.subject.meshNitric Oxide Synthase Type Iiien_US
dc.subject.meshNitroarginine - Pharmacologyen_US
dc.subject.meshSpecific Pathogen-Free Organismsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleAcetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout miceen_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.0702300en_US
dc.identifier.pmid10051139-
dc.identifier.scopuseid_2-s2.0-0032919816en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032919816&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume126en_US
dc.identifier.issue1en_US
dc.identifier.spage219en_US
dc.identifier.epage226en_US
dc.identifier.isiWOS:000078131000026-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChataigneau, T=6602561430en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridHuang, PL=7403659318en_US
dc.identifier.scopusauthoridFishman, MC=21634395600en_US
dc.identifier.scopusauthoridDuhault, J=7005108808en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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