Ischemia results in increased induction of 25 kD and 70 kD HSPs in renal cortex. Recent research suggests interactions of these HSPs with cytoskeletal elements during the restoration of cellular polarity. To determine whether pretreatment with ischemia protects the membrane-cytoskeletal complex after repeat renal ischemia, we investigated cellular distribution of 25 kD and 70 kD HSPs and of Na,K-ATPase after a single and after repeat ischemia (45 min) in rat renal cortex.

Male Sprague Dawley rats underwent either unilateral renal ischemia alone, or were pretreated with bilateral renal ischemia and, after 24 hours of reflow, were then subjected to unilateral renal ischemia. Renal cortex was fractionated into cytoskeletal and detergent soluble fraction by Triton X-100 extraction and immunodensitometrie was performed.

The HSPs re-distributed into the cytoskeletal fraction after single and repeat renal ischemia. Levels of 25 kD and 70 kD HSPs were significantly higher in renal cortex from pretreated animals. In contrast to single ischemia, repeat ischemia did not result in increased Triton-extractability of Na,K-ATPase.

These observations suggest that 25 kD and 70 kD HSPs increased their affinity for cytoskeletal elements after renal ischemia. Increased levels of these stressproteins might stabilize the membrane-cytoskeletal complex after repeat renal ischemia.