Role of endothelium-derived hyperpolarizing factor in shear stress-induced endothelium-dependent relaxations of rats / 药学学报
Acta Pharmaceutica Sinica
; (12): 491-495, 2005.
Article
in Zh
| WPRIM
| ID: wpr-353487
Responsible library:
WPRO
ABSTRACT
<p><b>AIM</b>To investigate the role and mechanism of endothelium-derived hyperpolarizing factor (EDHF) in shear stress induced vasorelaxation of rat mesenteric artery.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>EDHF plays an important role in shear stress-induced endothelium-dependent relaxations, and K channels especially calcium-activated K channels appear to be involved.</p>
Full text:
1
Database:
WPRIM
Main subject:
Apamin
/
Pharmacology
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Physiology
/
Proadifen
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Vasodilation
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In Vitro Techniques
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Endothelium, Vascular
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Biological Factors
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Rats, Wistar
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Charybdotoxin
Limits:
Animals
Language:
Zh
Journal:
Acta Pharmaceutica Sinica
Year:
2005
Document type:
Article