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Expression and molecular regulation of Na(+)-K(+)-ATPase after renal ischemia. Am J Physiol 1994 Jul;267(1 Pt 2):F75-85



Pubmed ID




Scopus ID

2-s2.0-0027990439   56 Citations


Renal ischemia causes redistribution of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) to the apical membrane of proximal tubules. We determined the time course of regeneration of Na(+)-K(+)-ATPase polarity and sought evidence of increased enzyme production during recovery as a means to restore polarity. Anesthetized rats underwent 45 min renal ischemia and reflow of 15 min, 2 h, 6 h, and 24 h. Immunofluorescent and electron microscopy showed loss of strict basolateral localization of Na(+)-K(+)-ATPase at 15 min reflow with repolarization by 24 h in sublethally injured cells. Both alpha 1- and beta-subunits were only in microsomal fractions at all reflow intervals. Immunodetectable levels of both subunits declined to 60-70% of control by 24 h reflow. Levels of mRNA for each subunit declined in parallel through 24 h to 55% of control. Overall transcription was profoundly depressed through 6 h but had recovered to near control by 24 h. Specific transcription of alpha 1- and beta-subunit mRNA was markedly decreased after ischemia and only partially recovered by 24 h. These results suggest that recycling of misplaced units rather than new Na(+)-K(+)-ATPase production is the means by which renal epithelia initially repolarize after ischemic injury.

Author List

Van Why SK, Mann AS, Ardito T, Siegel NJ, Kashgarian M


Scott K. Van Why MD Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Blotting, Northern
Blotting, Western
Cell Polarity
Microscopy, Electron
Protein Processing, Post-Translational
RNA, Messenger
Rats, Sprague-Dawley
Renal Circulation
Sodium-Potassium-Exchanging ATPase
Transcription, Genetic