It is known that HSP70 plays an important role in the antiischaemic effect of adaptation to stress. The aim of our study was to verify the hypothesis that nitric oxide (NO) may contribute to the activation of HSP70 synthesis and to enhance thereby the resistance of organism to the ischaemic and reperfusion damages. We observed that heat shock potentiated NO production in the heart NO formation was completely blocked by the NO synthase inhibitor N^-nitro-L-arginine (L-NNA). L-NNA also significantly attenuated the heat shock-induced accumulation of HSP70 (by 45 % in heart). Both heat shock and NO donor induced time- and concentration-dependent HSP70 synthesis in the culture of human hepatoblastoma cells Hep G2. Prior injection of NO donor (30-100 mg per rat) exerted a dose- dependent protective effect on the isolated heart in ischaemia and reperfusion within 24 hours. We suggest that NO is involved in the activation of HSP70 synthesis which can play an important role in the delayed protective effect of NO donors.
The stimulating effect of 1-alkyl-1-ethyl piperidinium bromides on the oxygen evolution rate in spinách chloroplasts was caused by rearrangement of thylakoid membrane.