In the present study, beta-endorphin (BE), beta-lipotropin (B-LPH) and the ratio of beta-endorphin to beta-lipotropin (BE:B-LPH) were determined in rat cardiac tissue in response to physical stress induced by immobilization and cardiovascular stress resulting from hemorrhagic shock and pressure overload-induced cardiac hypertrophy. As compared with controls, BE was increased and B-LPH was decreased in cardiac tissue from animals subjected to immobilization, and there was also a significant rise in the ratio of BE:B-LPH. Cardiac BE remained unchanged following hemorrhage, while B-LPH was diminished, resulting in an increase in the ratio of BE:B-LPH. Similarly, the concentration of BE was unchanged, the concentration of B-LPH was significantly diminished and the ratio of BE:B-LPH was significantly increased in hypertrophied hearts. Thus, immobilization-induced stress, hemorrhagic shock, and cardiac hypertrophy all increased the ratio of BE:B-LPH in the heart. However, it appears that immobilization stress induces an increase in cardiac BE, whereas cardiovascular stress results in a preservation of BE in the heart and a reduction in cardiac B-LPH. The data suggests that physical stress (induced by immobilization) and cardiovascular stress (i.e., hemorrhage, hypertrophy) have differential effects on the synthesis of BE and the post-translational processing of proopiomelanocortin in the heart. Furthermore, the alterations in cardiac tissue BE and possibly B-LPH may play a role in the response of the heart to physical and cardiovascular stress.

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