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Epithelial polarity following ischemia: a requirement for normal cell function.
D M Spiegel1, P D Wilson, B A Molitoris
1Division of Nephrology, Veterans Administration Medical Center, Denver, Colorado.
The American Journal of Physiology
|March 1, 1989
Summary
Kidney proximal tubule (PT) dysfunction after ischemia recovers only when surface membrane polarity is reestablished. This involves restoring lipid and protein polarity for normal glucose and sodium reabsorption.
Area of Science:
- Nephrology
- Cell Biology
- Renal Physiology
Background:
- Ischemic injury causes proximal tubule (PT) dysfunction and loss of surface membrane (SM) polarity.
- Epithelial vectorial transport relies on SM polarity.
Purpose of the Study:
- To determine if renal cortical PT dysfunction correction post-ischemia depends on SM polarity reestablishment.
- Investigate the role of SM polarity in functional recovery after acute renal failure.
Main Methods:
- Induction of acute renal failure via bilateral pedicle clamping (50 min).
- Assessment of serum creatinine, fractional sodium excretion, and fractional lithium clearances.
- Evaluation of PT cellular ultrastructure, glucose reabsorption, and Na+-K+-ATPase polarity (cytochemical and biochemical).
Main Results:
- Morphological recovery of PT occurred by day 3, but glucose reabsorption defects persisted.
- Delayed recovery of glucose handling correlated with apical membrane lipid polarity normalization.
- Ischemia caused Na+-K+-ATPase redistribution to the apical membrane; polarity normalized by day 8, paralleling Na+ reabsorption recovery.
Conclusions:
- Functional recovery of PT glucose and Na+ reabsorption post-ischemia requires morphological restoration and reestablishment of SM lipid and protein polarity.
- Apical Na+-K+-ATPase polarity is crucial for normal Na+ reabsorption following ischemic injury.