Impaired endothelial calcium signaling is responsible for the defective dilation of mesenteric resistance arteries from db/db mice to acetylcholine.

摘要: We aimed at assessing the role of endothelial cell calcium for dysfunction mesenteric resistance arteries db/db mice (a model type 2 diabetes) and determine whether treatment with sulfaphenazole, improves signaling function. Pressure myography was used to study acetylcholine (ACh) -induced vasodilation. Intracellular ([Ca(2+)]i) transients measured by confocal laser scanning microscopy smooth muscle membrane potential sharp microelectrodes. The impaired dilation ACh observed in from improved sulfaphenazole 8 weeks. associated decreased [Ca(2+)]i hyperpolarization. Sulfaphenazole applied vitro mediated both absence presence inhibitors nitric oxide cyclooxygenase. also increased percentage cells induced increases [Ca(2+)]i. shows that control can explain reduced function diabetic responses consequently endothelium-dependent These observations provide mechanistic insight into diabetes.