Please use this identifier to cite or link to this item:
|Title:||Role of PKC in the novel synergistic action of urotensin II and angiotensin II and in urotensin II-induced vasoconstriction|
|Keywords:||Protein kinase C|
Vascular smooth muscle cells
|Citation:||Wang, 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|
|Abstract:||The 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.|
|Source Title:||American Journal of Physiology - Heart and Circulatory Physiology|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 19, 2019
WEB OF SCIENCETM
checked on Feb 19, 2019
checked on Feb 8, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.