title: [Role of endothelium-derived hyperpolarizing factor in shear stress-induced endothelium-dependent relaxations of rats].
abstract: OBJECTIVE
  To investigate the role and mechanism of endothelium-derived hyperpolarizing factor (EDHF) in shear stress induced vasorelaxation of rat mesenteric artery.
  
  
  METHODS
  The changes in vessel diameter in response to variable flow (0-300 microL.min(-1)) were continuously examined. The contribution of prostacyclin (PGI2), NO and EDHF to shear stress induced relaxation were analyzed by inhibitory effects of indomethacin, N(G)-nitro-L-arginine (L-NA) and KCl. The nature and hyperpolarizing mechanism of EDHF were examined by the inhibitory effects of inhibitors of cytochrome P450 pathway and of various K+ channels.
  
  
  RESULTS
  The shear stress-induced relaxation were endothelium dependent and the contribution of NO was more prominent in large mesenteric arteries (400-500 microm) than that in resistance arteries (150-250 microm), whereas that of EDHF was noted in both-sized blood vessels. Tetrabutylammonium (a nonselective inhibitor of K channels) almost abolished, whereas the combination of charybdotoxin (an inhibitor of both large and intermediate-conductance Ca2+-activated K channels) and apamin (an inhibitor of small-conductance Ca2+-activated K channels) significantly inhibited the EDHF-mediated component of the shear stress-induced relaxations.
  
  
  CONCLUSIONS
  EDHF plays an important role in shear stress-induced endothelium-dependent relaxations, and K channels especially calcium-activated K channels appear to be involved.
authors.affiliation: Department of Cardiology, First Teaching Hospital, Jilin University, Changchun 130021, China. zhaohuiying163@163.com
authors.forename: Hui-Ying
authors.initials: HY
authors.lastname: Zhao
authors.forename: Quan
authors.initials: Q
authors.lastname: Liu
authors.forename: Bao-Rong
authors.initials: BR
authors.lastname: Chi
mesh_terms: D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001685:Biological Factors / Q000502:physiology*; D018999:Charybdotoxin / Q000494:pharmacology; D065607:Cytochrome P-450 Enzyme Inhibitors; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000037:antagonists & inhibitors; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011335:Proadifen / Q000494:pharmacology; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects
chemical_list: D001685:Biological Factors; D065607:Cytochrome P-450 Enzyme Inhibitors; D051036:Large-Conductance Calcium-Activated Potassium Channels; D026902:Potassium Channel Blockers; D000644:Quaternary Ammonium Compounds; D051640:Small-Conductance Calcium-Activated Potassium Channels; C067410:endothelium-dependent hyperpolarization factor; D018999:Charybdotoxin; D001030:Apamin; D009569:Nitric Oxide; D011335:Proadifen; C009405:tetrabutylammonium