Nitric oxide and K_ir6.1 potassium channel mediate isoquercitrin-induced endothelium-dependent and independent vasodilation in the mesenteric arterial bed of rats

详细信息    查看全文

• 作者：Arquimedes Gasparotto Junior^a ; ^{arquimedesgasparotto@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; Renê ; dos Reis Piornedo^b ; Jamil Assreuy^b ; José ; Eduardo Da Silva-Santos^b ; ^{j.e.silva.santos@ufsc.br" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Acetylcholine chloride (Pubchem CID 6060) ; Glibenclamide (PubChem CID ; 3488) ; Iberiotoxin (PubChem CID 16132435) ; Indomethacin (PubChem CID 3715) ; Isoquercitrin (PubChem CID 5280804) ; N-Nitroarginine methyl ester (PubChem CID 39836) ; Phenylephrine hydrochloride (PubChem CID ; 5284443) ; Tetraethylammonium chloride (PubChem CID 5946)
• 刊名：European Journal of Pharmacology
• 出版年：2016
• 出版时间：5 October 2016
• 年：2016
• 卷：788
• 期：Complete
• 页码：328-334
• 全文大小：410 K

文摘

The vascular effect of flavonoid isoquercitrin was investigated in the perfused mesenteric vascular bed of rats. In preparations with functional endothelium isoquercitrin (100, 300 and 1000 nmol) dose-dependently reduced the perfusion pressure by 13±2.2, 33±3.9, and 58±3.7 mm Hg, respectively. Endothelium removal or inhibition of the nitric oxide synthase enzymes by l-NAME did not change the effects of 100 and 300 nmol isoquercitrin, but reduced by 30–40% the vasodilation induced by 1000 nmol isoquercitrin. Perfusion with nutritive solution containing 40 mM KCl abolished the vasodilatory effect of all isoquercitrin doses. Treatment with glibenclamide, a K_ir6.1 (ATP-sensitive) potassium channel blocker, inhibited vasodilation induced by 100 and 300 nmol isoquercitrin, but only partially reduced the effect of 1000 nmol isoquercitrin. The non-selective K_Ca (calcium-activated) potassium channel blocker tetraethylammonium, but not the selective K_Ca1.1 channel blocker iberiotoxin, reduced by around 60% vasodilation induced by all isoquercitrin doses. In addition, association of tetraethylammonium and glibenclamide, or l-NAME and glibenclamide, fully inhibited isoquercitrin-induced vasodilation. Our study shows that isoquercitrin induces vasodilation in resistance arteries, an effect mediated by K⁺ channel opening and endothelial nitric oxide production.