| Cheng, YW., Li, C.H., Lee, C.C. and Kang, J.J. |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol=368 ------>confirm_bywho=kyhsu ------>insert_bywho=ywcheng ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=385 ------>medlineContent= ------>unit=G0100 ------>insert_date=20030916 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=7 ------>ISSN=None ------>authors_c=None ------>score=397 ------>journal_name=Naunyn-Schmiedeberg's Archives of Pharmacology. ------>paper_name=Alpha-Naphthoflavone Induced Vasorelaxation Through the Induction of Extracellular Calcium Influx and Nitric Oxide Formation in Endothelium ------>confirm_date=20040413 ------>tch_id=089070 ------>pmid=14564451 ------>page1=377 ------>fullAbstract=The effect of alpha-naphthoflavone (alpha-NF) on vascular function was studied in isolated ring segments of the rat thoracic aorta and in primary cultures of human umbilical vein endothelial cells (HUVECs). alpha-NF induced concentration-dependent relaxation of the phenylephrine-precontracted aorta endothelium-dependently and -independently at lower and higher concentrations, respectively. The cGMP, but not cAMP, content was increased significantly in alpha-NF-treated aorta. Pretreatment with N(omega)-nitro- l-arginine methyl ester (L-NAME) or methylene blue attenuated both alpha-NF induced vasorelaxation and the increase of cGMP content significantly. The increase of cGMP content induced by alpha-NF was also inhibited by chelating extracellular Ca(2+) with EGTA. These results suggest that the endothelium-dependent vasorelaxation induced by alpha-NF is mediated most probably through Ca(2+)-dependent activation of NO synthase and guanylyl cyclase. In HUVECs, alpha-NF induced concentration-dependent formation of NO and Ca(2+) influx. alpha-NF-induced NO formation was abolished by removal of extracellular Ca(2+) and by pretreatment with the Ca(2+) channel blockers SKF 96365 and Ni(2+), but not by the L-type Ca(2+) channel blocker verapamil. The Ca(2+) influx, as measured by (45)Ca(2+) uptake, induced by alpha-NF was also inhibited by SKF 96365 and Ni(2+). Our data imply that alpha-NF, at lower concentrations, induces endothelium-dependent vasorelaxation by promoting extracellular Ca(2+) influx in endothelium and the activation of the NO-cGMP pathway. ------>tmu_sno=None ------>sno=7554 ------>authors2= ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Cheng, YW., Li, C.H., Lee, C.C. and Kang, J.J. ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Alpha-naphthoflavone induces vasorelaxation through the induction of extracellular calcium influx and NO formation in endothelium. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no=5 ------>patent_SDate=None ------>update_bywho= ------>publish_year=2003 ------>submit_flag= ------>publish_month=None |