Details

Autor(en) / Beteiligte

• Zhou, Zi Qi
• Sun, Sha Sha
• Zhou, Guang Hai
• Kang, Dae Gill
• Lee, Ho Sub
• Yang, Sun Nye
• Cho, Kyung Woo
• Jin, Song Nan
• Wen, Jin Fu

Titel

Physcion Induces Vasorelaxation In Rat Aorta through Endothelium‐dependent and Endothelium‐independent Mechanisms

Ist Teil von

• The FASEB journal, 2016-04, Vol.30 (S1)

Erscheinungsjahr

2016

Link zum Volltext

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• Abstract only Background Physcion, an active anthraquinone constituent isolated from the rhubarb, a traditional Chinese herbal medicine which is widely used in clinical treatment, has cardiovascular protective properties. However, the effects of physcion on the vascular function and its pharmacological mechanisms of action have not been studied. The aim of the present study was to evaluate the vascular effects of physcion and its action mechanisms in rats. Methods and Results Aortic rings from Sprague‐Dawley rats were mounted in organ baths, and the effects of physcion on vascular function were studied by means of isometric tension recording. Physcion induced a concentration‐dependent relaxation of pre‐contracted aortic rings in endothelium‐intact (+E) and endothelium‐denuded (−E) vessels. The nitric oxide synthase inhibitor L‐NAME, as well as the soluble guanylate cyclase inhibitor ODQ, attenuated the relaxation in +E but not in −E vessels. Inhibition of cyclooxygenases with indomethacin had no effects on the physcion‐induced vasorelaxation in +E vessels. A modulator of the store‐operated Ca 2+ entry (SOCE), 2‐aminoethyl diphenylborinate markedly attenuated the physcion‐induced vasorelaxation in +E vessels. In −E preparations, K + channel blockers, such as tetraethylammonium, large‐conductance calcium‐activated K + (K Ca ) channel blocker iberiotoxin, and K ATP channel blocker glibenclamide significantly attenuated the relaxation elicited by physcion. Conclusions These data demonstrate that physcion induces vasorelaxation through activation of endothelium‐dependent and ‐independent signaling pathways: endothelium‐dependent NO‐cGMP signaling and endothelium‐independent K Ca channel and K ATP channel signaling. Support or Funding Information Acknowledgments: This work was supported by research grants from the National Natural Science Foundation of China (Nos. 81270920, 31571175), the Natural Science Foundation of Shandong Province (No. ZR2015HM037).