Please use this identifier to cite or link to this item: https://doi.org/10.1152/ajpheart.00512.2006
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dc.titleRole of PKC in the novel synergistic action of urotensin II and angiotensin II and in urotensin II-induced vasoconstriction
dc.contributor.authorWang, Y.-X.
dc.contributor.authorDing, Y.-J.
dc.contributor.authorZhu, Y.-Z.
dc.contributor.authorShi, Y.
dc.contributor.authorYao, T.
dc.contributor.authorZhu, Y.-C.
dc.date.accessioned2016-11-17T08:39:05Z
dc.date.available2016-11-17T08:39:05Z
dc.date.issued2007-01
dc.identifier.citationWang, Y.-X., Ding, Y.-J., Zhu, Y.-Z., Shi, Y., Yao, T., Zhu, Y.-C. (2007-01). Role of PKC in the novel synergistic action of urotensin II and angiotensin II and in urotensin II-induced vasoconstriction. American Journal of Physiology - Heart and Circulatory Physiology 292 (1) : H348-H359. ScholarBank@NUS Repository. https://doi.org/10.1152/ajpheart.00512.2006
dc.identifier.issn03636135
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/130601
dc.description.abstractThe intracellular signaling of human urotensin II (hU-II) and its interaction with other vasoconstrictors such as ANG II are poorly understood. In endothelium-denuded rat aorta, coadministration of hU-II (1 nM) and ANG II (2 nM) exerted a significant contractile effect that was associated with increased protein kinase C (PKC) activity and phosphorylation of PKC-α/βII and myosin light chain, whereas either hU-II or ANG II administered alone at these concentrations had no statistically significant effect. This synergistic effect was abrogated by the PKC inhibitor chelerythrine (10 and 30 μM), the selective PKC-α/βII inhibitor Gö-6976 (0.1 and 1 μM), the hU-II receptor ligand urantide (30 nM and 1 μM), or the ANG II antagonist losartan (1 μM). Moreover, in endothelium-intact rat aorta, the synergistic effect of hU-II and ANG II was not exerted any longer, and this synergistic effect was unmasked by pretreatment of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester. hU-II (10 nM) alone caused a long-lasting increase in phospho-PKC-θ, phospho-myosin light chain, and PKC activity, which was associated with long-lasting vasoconstriction. These changes were prevented by chelerythrine. Methoxyverapamil-thapsigargin treatment reduced the hU-II-induced vasoconstriction by ∼50%. The methoxyverapamil-thapsigargin-resistant component of hU-II-induced vasoconstriction was dose-dependently inhibited by chelerythrine. In conclusion, hU-II induces a novel PKC-dependent synergistic action with ANG II in inducing vasoconstriction. PKC-α/βII is probably the PKC isoform involved in this synergistic action. Nitric oxide produced in the endothelium probably masks this synergistic action. The long-lasting vasoconstriction induced by hU-II alone is PKC dependent and associated with PKC-θ phosphorylation. Copyright © 2007 the American Physiological Society.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1152/ajpheart.00512.2006
dc.sourceScopus
dc.subjectProtein kinase C
dc.subjectVascular smooth muscle cells
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1152/ajpheart.00512.2006
dc.description.sourcetitleAmerican Journal of Physiology - Heart and Circulatory Physiology
dc.description.volume292
dc.description.issue1
dc.description.pageH348-H359
dc.description.codenAJPPD
dc.identifier.isiut000243383300042
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