TY - JOUR
T1 - The Results of Exposure to Immobilization, Hemorrhagic Shock, and Cardiac Hypertrophy on β-Endorphin in Rat Cardiac Tissue
AU - Forman, L. J.
AU - Hock, C. E.
AU - Harwell, M.
AU - Estilow-Isabell, S.
PY - 1994/6
Y1 - 1994/6
N2 - In the present study, β-endorphin (BE), β-lipotropin (B-LPH) and the ratio of β-endorphin to β-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.
AB - In the present study, β-endorphin (BE), β-lipotropin (B-LPH) and the ratio of β-endorphin to β-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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U2 - 10.3181/00379727-206-43730
DO - 10.3181/00379727-206-43730
M3 - Article
C2 - 8208735
AN - SCOPUS:0028246346
SN - 0037-9727
VL - 206
SP - 124
EP - 129
JO - Proceedings of the Society for Experimental Biology and Medicine
JF - Proceedings of the Society for Experimental Biology and Medicine
IS - 2
ER -