Na+/K(+)-ATPase activity in vascular smooth muscle from streptozotocin diabetic rat.
Na+/K(+)-ATPase activity in vascular smooth muscle from streptozotocin diabetic rat.
复制标题
链脲佐菌素糖尿病大鼠血管平滑肌中Na /K( )-ATP酶活性。
DOI：
10.1016/s0008-6363(96)00238-6
复制
发表时间：
1997
影响因子：
10.8
通讯作者：
Solar,SM
中科院分区：
文献类型：
--
作者：
Smith,JM;Paulson,DJ;Solar,SM
目的：胰岛素缺乏型糖尿病损害多种组织的碳水化合物代谢。血管平滑肌可能对糖尿病引起的糖酵解紊乱敏感，因为该组织中的Na+/K+-ATP酶优先利用糖酵解产生的ATP。本研究的目的是确定是否慢性暴露于胰岛素缺乏型糖尿病相关的代谢改变直接抑制Na+/K+-ATP酶活性，或其调节，在血管smoothmuscles.Methods：糖尿病是由静脉注射链脲佐菌素（60 mg/kg）。12周后，在各种条件下测定主动脉和上级肠系膜动脉Na+/K+-ATP酶活性。Na +/K +-ATP酶抑制剂哇巴因存在或不存在时，通过测量铷-86（86 Rb）的内流来估计Na+/K+-ATP酶。[3 H]葡萄糖和[14 C]葡萄糖的代谢分别用于估计糖酵解或葡萄糖氧化，结果：在主动脉平滑肌中，糖酵解和葡萄糖氧化减少（分别为27%和34%）。完整的内皮细胞与糖尿病主动脉中哇巴因敏感（泵介导）的86 Rb摄取显著减少相关。然而，哇巴因敏感的86 Rb摄取是相似的去内皮化的主动脉和上级肠系膜动脉糖尿病和非糖尿病大鼠在未刺激的条件下，并在最大刺激。去除葡萄糖或氧气减少哇巴因敏感的86 Rb摄取在两组相似的程度。与此相反，受体介导的哇巴因敏感的86 Rb摄取insulin.Conclusions的刺激：这些结果表明，内在的Na+/K+-ATP酶活性在生理条件下，糖尿病血管平滑肌细胞代谢的损害并没有减少限制刺激Na+/K+-ATP酶活性。然而，在糖尿病大鼠主动脉中，内皮因子或胰岛素对Na+/K+-ATP酶活性的调节似乎发生了改变。
Objectives:Insulin-deficient diabetes impairs carbohydrate metabolism in a variety of tissues. Vascular smooth muscle may be susceptible to the diabetes-induced disturbance in glycolysis since Na+/K+-ATPase in this tissue preferentially utilizes ATP generated by glycolysis. The purpose of this study was to determine if chronic exposure to the metabolic alterations associated with insulin-deficient diabetes directly inhibited Na+/K+-ATPase activity, or its regulation, in vascular smooth muscle.Methods:Diabetes was induced by intravenous administration of streptozotocin (60 mg/kg). After 12 weeks, Na+/K+-ATPase activity in aorta and superior mesenteric artery was evaluated under a variety of conditions. Na+/K+-ATPase was estimated by measuring the influx of rubidium-86 (86Rb) in the presence or absence of the Na+/K+-ATPase inhibitor, ouabain. The metabolism of [3H]glucose and [14C]glucose was used to estimate glycolysis or glucose oxidation, respectively.Results:Glycolysis and glucose oxidation were decreased in aortic smooth muscle (27 and 34%, respectively). An intact endothelium was associated with a marked decrease in ouabain-sensitive (pump-mediated)86Rb uptake in diabetic aorta. However, ouabain-sensitive86Rb uptake was similar in de-endothelialized aorta and superior mesenteric artery from diabetic and non-diabetic rats under both unstimulated conditions and during maximal stimulation. Removal of glucose or oxygen reduced ouabain-sensitive86Rb uptake to a similar extent in both groups. In contrast, the receptor-mediated stimulation of ouabain-sensitive86Rb uptake by insulin was decreased.Conclusions:These results suggest that intrinsic Na+/K+-ATPase activity is not diminished in diabetic vascular smooth muscle under physiological conditions and that the impairment of cellular metabolism in diabetic blood vessels does not limit stimulation of Na+/K+-ATPase activity. However, modulation of Na+/K+-ATPase activity by endothelial factors or insulin appears to be altered in aorta from diabetic rats.