Role of endothelium-derived hyperpolarizing factor in shear stress-induced endothelium-dependent relaxations of rats.
- Author:
Hui-Ying ZHAO
1
;
Quan LIU
;
Bao-Rong CHI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apamin; pharmacology; Biological Factors; physiology; Charybdotoxin; pharmacology; Cytochrome P-450 Enzyme Inhibitors; Endothelium, Vascular; drug effects; physiology; In Vitro Techniques; Large-Conductance Calcium-Activated Potassium Channels; antagonists & inhibitors; Male; Mesenteric Arteries; drug effects; physiology; Nitric Oxide; physiology; Potassium Channel Blockers; pharmacology; Proadifen; pharmacology; Quaternary Ammonium Compounds; pharmacology; Rats; Rats, Wistar; Small-Conductance Calcium-Activated Potassium Channels; antagonists & inhibitors; Vasodilation; drug effects
- From: Acta Pharmaceutica Sinica 2005;40(6):491-495
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the role and mechanism of endothelium-derived hyperpolarizing factor (EDHF) in shear stress induced vasorelaxation of rat mesenteric artery.
METHODSThe 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.
RESULTSThe 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.
CONCLUSIONEDHF plays an important role in shear stress-induced endothelium-dependent relaxations, and K channels especially calcium-activated K channels appear to be involved.
