Original ArticleNitric Oxide and Catalase-sensitive Relaxation by Scutellarin in the Mouse Thoracic AortaYang, Weimin MD, PhD*†; Lust, Robert M PhD*; Bofferding, April BS*; Wingard, Christopher J PhD*Author Information From the *Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC; and †Yunnan Pharmacological Laboratories of Natural Products, Kunming Medical College, Kunming, China. Received for publication November 20, 2007; accepted November 19, 2008. Supported in part by a Mid-Atlantic AHA affiliate postdoctoral fellowship and the Department of Yunnan Provincial Education Visiting Scholarship awarded to W.Y. and other support from Philip Morris, USA, and International awarded to C.J.W. Reprints: Christopher J. Wingard, PhD, Department of Physiology, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Room 6E98, Greenville, NC 27834 (e-mail: firstname.lastname@example.org). Journal of Cardiovascular Pharmacology: January 2009 - Volume 53 - Issue 1 - p 66-76 doi: 10.1097/FJC.0b013e318195d776 Buy Metrics Abstract The vascular activity of scutellarin (SCU), a flavonoid isolated from a Chinese traditional medicinal plant, was investigated in isolated thoracic aortic rings of mice. SCU-induced dose-dependent relaxation of phenylephrine (1 μM) stimulated contractions. This relaxation was reduced by endothelium removal, significantly reduced by both the nitric oxide synthase inhibitor (Nω-nitro-l-arginine methylester, 300 μM) and slightly limited by the soluble guanylyl cyclase inhibitor (1 H-[1,2,4] oxidazolol [4,3-a] quinoxalin-1-one, 100 μM). The catalase inhibitor (3-amino-1,2,4-triazole, 50 mM) augmented the constriction and blocked the lowest SCU concentration relaxation, whereas catalase addition was without effect. Preincubation with 300 and 1000 μM SCU significantly suppressed the contractile dose-response to phenylephrine, causing both a significant rise in half maximal effective concentration and a decrease in the maximal developed force. Western blot analysis showed that SCU inhibition of contraction was independent of reductions in myosin light chain phosphorylation. These results suggested that SCU relaxation was predominantly endothelium dependent and likely involved the catalase-sensitive nitric oxide synthase signaling pathway, without loss of myosin phosphorylation. The potential clinical use of SCU may prove to be effective in increasing vasoreactivity, independently of smooth muscle contractile activity that is mediated by the 20-kDa myosin light chain phosphorylation. © 2009 Lippincott Williams & Wilkins, Inc.