Role of heat stress response in the tolerance of immature renal tubules to anoxia

The stress response was studied in suspensions of tubules from immature (IT) and mature (MT) rats after noninjury, heat, oxygen, and anoxia. Under all conditions, IT exhibited more exuberant activation of heat shock transcription factor (HSF) than MT. Characterization of activated HSF in immature cortex revealed HSF1. Also, 2 h after each condition, heat shock protein-72 (HSP-72) mRNA was twofold in IT. As the metabolic response to 45 min of anoxia, 20-min reoxygenation was assessed by measuring O(2) consumption (O(2)C). Basal O(2)C was manipulated with ouabain, nystatin, and carbonylcyanide p-chloromethyoxyphenylhydrazone (CCCP). Basal O(2)C in IT were one-half the value of MT. After anoxia, basal O(2)C was reduced by a greater degree in MT. Ouabain reduced O(2)C to half the basal value in both noninjured and anoxic groups. Basal O(2)C was significantly stimulated by nystatin but not to the same level following anoxia in MT and IT. Basal O(2)C was also stimulated by CCCP, but after anoxia, CCCP O(2)C was significantly less in MT with no decrease in IT, suggesting mitochondria are better preserved in IT. Also, O(2)C devoted to nontransport activity was better maintained in IT.