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dc.contributor.authorEguchi, Daihiko
dc.contributor.authord'Uscio, Livius V.
dc.contributor.authorWambi, Chris
dc.contributor.authorWeiler, Deborah
dc.contributor.authorKovesdi, Imre
dc.contributor.authorO'Brien, Timothy
dc.contributor.authorKatusic, Zvonimir S.
dc.date.accessioned2018-08-24T08:24:41Z
dc.date.available2018-08-24T08:24:41Z
dc.date.issued2002-08-22
dc.identifier.citationEguchi, Daihiko; d'Uscio, Livius V. Wambi, Chris; Weiler, Deborah; Kovesdi, Imre; O'Brien, Timothy; Katusic, Zvonimir S. (2002). Inhibitory effect of recombinant inos gene expression on vasomotor function of canine basilar artery. American Journal of Physiology - Heart and Circulatory Physiology 283 (6), H2560-H2566
dc.identifier.issn0363-6135,1522-1539
dc.identifier.urihttp://hdl.handle.net/10379/9100
dc.description.abstractThe present study was designed to determine the effect of recombinant inducible nitric oxide (NO) synthase (iNOS) gene expression on vasomotor function in cerebral arteries. Isolated canine basilar arteries were exposed ex vivo (30 min at 37degreesC) to an adenoviral vector [10(7), 10(8), or 10(9) plaque-forming units (pfu)/ml] encoding either the iNOS gene or the beta-galactosidase reporter gene. Twenty-four hours after transduction, Western blot analysis demonstrated expression of iNOS protein only in iNOS (10(9) pfu/ml)-transduced arteries. Immunohistochemical analysis localized iNOS expression predominantly in adventitia. Vascular reactivity of isolated basilar arteries was studied by isometric force recording. Concentration-response curves to UTP (10(-9)-10(-3) M) and diethylaminodiazen-1-ium-1,2-dioate (10(-10)-10(-5) M) were significantly shifted to the right in iNOS gene (109 pfu/ml)-transduced rings compared with control and beta-galactosidase-transduced rings (P < 0.05, n = 5-6). Endothelium-dependent relaxation to bradykinin was significantly attenuated in iNOS-transduced rings (P < 0.001, n = 8). The basal level of cGMP and superoxide anion (O-2(-).) production were elevated in iNOS-transduced rings (P < 0.05, n = 7 for cGMP; P < 0.01, n = 6-9 for O-2(-). production). Our results suggest that expression of recombinant iNOS in cerebral arteries reduces vasomotor reactivity to both vasoconstrictor and vasodilator agonists. Attenuation of contractions is most likely due to functional antagonism between UTP and cGMP. Reduction of endothelium-dependent relaxation to bradykinin appears to be mediated in part by reduced reactivity of smooth muscle cells to NO.
dc.publisherAmerican Physiological Society
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiology
dc.subjectadventitia
dc.subjectbradykinin
dc.subjectnitric oxide
dc.subjectsuperoxide anion
dc.subjectinducible nitric oxide synthase
dc.subjectnitric-oxide synthase
dc.subjectendothelium
dc.subjectadventitia
dc.subjectsuperoxide
dc.subjectvivo
dc.subjectmice
dc.subjectatherosclerosis
dc.subjectvasorelaxation
dc.subjectdeficiency
dc.subjectvalidation
dc.titleInhibitory effect of recombinant inos gene expression on vasomotor function of canine basilar artery
dc.typeArticle
dc.identifier.doi10.1152/ajpheart.00415.2002
dc.local.publishedsourcehttp://ajpheart.physiology.org/content/ajpheart/283/6/H2560.full.pdf
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