[The limitation of acute hypotension and hyperactivation of the vascular endothelium in rats with an experimental myocardial infarct by using preliminary adaptation to physical load].

Adaptation to swimming exercise was shown to increase the endothelium-dependent relaxation of the rat aorta, leaving the BP unaffected. In experimental myocardial infarction, the adaptation limited the BP fall and completely prevented an excessive suppression of norepinephrine-induced contractions of the aorta. An adaptation to exercise seems to be an efficient protective factor in pathological conditions involving the NO overproduction and endothelial hyperactivation.

[The effect of adaptation to a physical load on the endothelium-mediated reactions of isolated vessels and NO production in rats].

Adaptation to exercise exerts a beneficial therapeutic and protective effect in several cardiovascular diseases many of which are characterized by disorders of endothelium-dependent vascular responses. To evaluate a possible role of functional condition of the endothelium in protective effects of adaptation to exercise we studied the effect of such adaptation on endothelium-dependent constrictor and dilator responses of the isolated rat aorta and on nitric oxide (NO) production in the organism. It was shown that adaptation to exercise (swimming) increased the suppression by the endothelium of constrictor responses to norepinephrine and potentiated the endothelium-dependent relaxation to acetylcholine.

The role of hsp70 and IP3-DAG mechanism in the adaptive stabilization of structures and heart protection.

This study has shown that the maximal activation of the IP3-DAG regulatory circuit is observed on the 14th day of adaptation to repeated stresses. This activation is characterized by increased activity of phospholipase C and of the positive inotropic response of isolated heart to an alpha-agonist. Simultaneously, this activation is accompanied by the accumulation of five heat shock protein 70 (hsp70) isoforms.