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• W2087657106 abstract "Impaired endothelial function, which is dysregulated in diabetes, also precedes hypertension. We hypothesized that in Type 2 diabetes, the impaired endothelium-dependent relaxation is due to a loss of endothelium-derived hyperpolarization (EDH) that is regulated by impaired ion channel function. Zucker diabetic fatty (ZDF), Zucker heterozygote, and homozygote lean control rats were used as the experimental models in our study. Third-order mesenteric arteries were dissected and mounted on a pressure myograph; mRNA was quantified by RT-PCR and channel proteins by Western blotting. Under nitric oxide (NO) synthase and cyclooxygenase inhibition, endothelial stimulation with ACh fully relaxes control but not diabetic arteries. In contrast, when small-conductance calcium-activated potassium (K Ca ) channels and intermediate- and large-conductance K Ca (I/BK Ca ) are inhibited with apamin and charybdotoxin, NO is able to compensate for ACh-induced relaxation in control but not in diabetic vessels. After replacement of charybdotoxin with 1-[(2-chlorophenyl)diphenylmethyl]- 1 H-pyrazole (TRAM-34; IK Ca inhibitor), ACh-induced relaxation in diabetic animals is attenuated. Specific inhibition with TRAM-34 or charybdotoxin attenuates ACh relaxation in diabetes. Stimulation with 1-ethyl-2-benzimidazolinone (IK Ca activator) shows a reduced relaxation in diabetes. Activation of BK Ca with 1,3-dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)- 2 H-benzimidazol-2-one NS619 leads to similar relaxations of control and diabetic arteries. RT-PCR and Western blot analysis demonstrate elevated mRNA and protein expression levels of IK Ca in diabetes. Our results suggest that the compensatory effect of NO and EDH-associated, endothelium-dependent relaxation is reduced in ZDF rats. Specific blockade of IK Ca with TRAM-34 reduces NO and EDH-type relaxation in diabetic rats, indicating an elevated contribution of IK Ca in diabetic small mesenteric artery relaxation. This finding correlates with increased IK Ca mRNA and protein expression in this vessel." @default.
• W2087657106 created "2016-06-24" @default.
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• W2087657106 date "2014-10-15" @default.
• W2087657106 modified "2023-10-09" @default.
• W2087657106 title "Type 2 diabetes: increased expression and contribution of IK_Ca channels to vasodilation in small mesenteric arteries of ZDF rats" @default.
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• W2087657106 doi "https://doi.org/10.1152/ajpheart.00240.2013" @default.
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