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      Cortical Na +,K +-ATPase Activity, Abundance and Distribution after in vivo Renal Ischemia without Reperfusion in Rats


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          The aim of our work was to study the changes in activity, abundance and distribution of sodium, potassium-adenosine triphosphatase (Na<sup>+</sup>,K<sup>+</sup>-ATPase) in membranes of cortical tubular cells in an in vivo model of ischemic injury without reperfusion. Na<sup>+</sup>,K<sup>+</sup>-ATPase, alkaline phosphatase (AP) activities and their distribution in membranes isolated from renal cortex using a Percoll gradient were studied after different ischemic periods. Na<sup>+</sup>,K<sup>+</sup>-ATPase α-subunit protein abundance was analysed by Western-blot. Plasma urea and cortical adenosine 5’triphosphate (ATP) were also measured. In cortical homogenates 5 min of ischemia promoted a diminution in ATP content. Na<sup>+</sup>,K<sup>+</sup>-ATPase activity diminished after 40 min and AP after 100 min of ischemia. Na<sup>+</sup>,K<sup>+</sup>-ATPase activity in the Percoll gradient fractions after 5 min peaked at a higher density and was significantly decreased after 40 min. AP activity was decreased in typically enriched apical membranes after both times of ischemia. At each time studied Na<sup>+</sup>,K<sup>+</sup>-ATPase abundance was increased in cortical homogenates and membranes. Our results showed opposite effects of ischemia on Na<sup>+</sup>,K<sup>+</sup>-ATPase activity and abundance. Increased levels of Na<sup>+</sup>,K<sup>+</sup>-ATPase protein were observed. The enzyme would be rapidly delivered to membrane domains and become inactivated as ischemia persists.

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          Alterations in epithelial polarity and the pathogenesis of disease states.

          The establishment and maintenance of epithelial-cell polarity are prerequisites for normal epithelial-cell and organ function. Knowledge of the processes involved in cell polarity has provided insight into the mechanisms of cell dysfunction and the pathogenesis of several diseases. These insights should lead to the development of specific strategies aimed at preventing or minimizing the progression of these diseases.
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            Phosphorylation of the Catalyic α-Subunit Constitutes a Triggering Signal for Na+,K+-ATPase Endocytosis


              Author and article information

              S. Karger AG
              24 August 2001
              : 89
              : 1
              : 82-89
              Farmacología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Rosario, República Argentina
              46048 Nephron 2001;89:82–89
              © 2001 S. Karger AG, Basel

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              Page count
              Figures: 2, Tables: 1, References: 44, Pages: 8
              Self URI (application/pdf): https://www.karger.com/Article/Pdf/46048
              Self URI (text/html): https://www.karger.com/Article/FullText/46048
              Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
              Original Paper

              Cardiovascular Medicine,Nephrology
              Acute renal failure,Cortical tubular membranes,Na+,K+-ATPase,Ischemia,Rat kidney


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