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  • Title: Na+/K(+)-ATPase activity in vascular smooth muscle from streptozotocin diabetic rat.
    Author: Smith JM, Paulson DJ, Solar SM.
    Journal: Cardiovasc Res; 1997 Apr; 34(1):137-44. PubMed ID: 9217883.
    Abstract:
    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-sensitive 86Rb 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-sensitive 86Rb uptake to a similar extent in both groups. In contrast, the receptor-mediated stimulation of ouabain-sensitive 86Rb 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.
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