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Preconditioning cardioprotection is mediated by heat shock protein 70 (HSP70). Increased intracellular calcium ([Ca2+]i) causes damage, and lowering it is thought to be responsible for cardioprotection. Preconditioning of HSP70 may restore [Ca2+]i homeostasis damaged by ischemic insult by lessening the defective handling of Ca2+ at various sites, as we expected. HSP70 activation was found to be effective.
When testosterone levels and the expression of HSP70, a stress response gene, decline with age, the effects of preconditioning are reduced or eliminated. To explain the delayed cardio protection, it was hypothesized that testosterone at physiological quantities is essential for HSP70 activation during preconditioning.
This hypothesis was tested in three different ways in male SD rats: the causal link between HSP70 activity and lower [Ca2+]i overload, the effects of HSP70 activation on Ca2+ handling at diverse sites, and (iii) the involvement of testosterone in HSP70 activation and cardio protection.