K(ATP)-mediated vasodilation is impaired in obese Zucker rats

肥胖 Zucker 大鼠的 K(ATP) 介导的血管舒张功能受损

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作者:Benjamin L Hodnett, Lusha Xiang, Jennifer A Dearman, Cory B Carter, Robert L Hester

Conclusion

The impaired functional vasodilation in the OZR is associated with altered K(ATP) channel sensitivity.

Methods

K(ATP) channel function was determined in isolated skeletal muscle arterioles in response to the K(ATP) opener cromakalim (0.1-10 microM) during normal myogenic tone and alpha-adrenergic-mediated tone (0.1 microM phenylephrine). The spinotrapezius muscle was prepared and the vasodilatory responses to muscle stimulation or iloprost (0.028-2.8 microM) were observed before and after the application of the K(ATP) inhibitor, glibenclamide (10 microM). Channel subunit expression was determined by using western blot analyses.

Objective

Skeletal muscle blood flow during exercise is impaired in obesity. We tested the hypothesis that the attenuated vasodilation in skeletal muscle arterioles of obese Zucker rats (OZR) is due to altered K(ATP) channel-mediated vasodilation. Materials and

Results

Cromakalim concentration-response curves were shifted in OZR as compared to lean controls. OZR exhibited impaired functional and iloprost-induced vasodilation as compared to the lean controls. Glibenclamide inhibited the functional and iloprost-induced dilation in the lean rats with no effects in the obese a nimals. Channel subunit expression was similar in femoral arteries.

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