Impaired BKCa channel function in native vascular smooth muscle from humans with type 2 diabetes.
作者： Madeline Nieves-Cintrón , Arsalan U. Syed , Olivia R. Buonarati , Robert R. Rigor , Matthew A. Nystoriak
DOI: 10.1038/S41598-017-14565-9
关键词:
摘要: Large-conductance Ca2+-activated potassium (BKCa) channels are key determinants of vascular smooth muscle excitability. Impaired BKCa channel function through remodeling β1 expression and contributes to complications in animal models diabetes. Yet, whether similar alterations occur native from humans with type 2 diabetes is unclear. In this study, we evaluated small resistance adipose arteries non-diabetic clinically diagnosed diabetic patients. We found that activity opposes pressure-induced constriction human adipose arteries, compromised Consistent impairment function, the amplitude frequency spontaneous currents, but not Ca2+ sparks were lower cells exhibited reduced sensitivity, single-channel open probability tamoxifen sensitivity. These effects associated decreased functional coupling between α subunits, no change total protein abundance. Overall, results suggest patients unique mechanisms, which may contribute
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