The Results of Exposure to Immobilization, Hemorrhagic Shock, and Cardiac Hypertrophy on  -Endorphin in Rat Cardiac Tissue

Abstract

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.

Cardiac Opioids

“…Cardiac tissue and isolated cardiac myocytes contain dynorphins and prodynorphin mRNA (13, 14), enkephalins and proenkephalin mRNA (15, 16), and β‐endorphin and pro‐opiomelanocortin mRNA (17–19). In addition, physiological conditions regulate the message and the peptide products.…”

Detection of nonopioid β‐endorphin receptor in the rat myocardium

“…They also reported that the ratio of b-endorphin to b-lipotropin is influenced by hemorrhagic shock, cardiac hypertrophy and other physiological stimuli, providing evidence that POMC processing can be regulated in heart [26]. Forman and Bagasra [27] were also the first to provide evidence that POMC may be synthesized by cardiomyocytes. They reported that POMC messenger RNA (mRNA) is detectable in ventricular myocytes by in situ hybridization histochemistry using an oligonucleotide probe corresponding to the POMC gene sequence encoding b-endorphin's N-terminus [28].…”

Opioid gene expression in the developing and adult rat heart

“…A number of publications have documented that the opioid peptide, ␤-endorphin, derived from POMC, can be detected in the adult rat heart (Ng and Ng, 1990;Millington et al, 1993;Forman et al, 1994). Moreover, POMC mRNA has been found in the heart by Forman and Bagasra (1992), suggesting an autocrine production of this neuropeptide.…”

“…Endogenous opioids serve in neuromodulation (Akil et al, 1984), and play a role in the growth processes of normal, neoplastic, renewing, and healing tissues (e.g., McLaughlin, 1994McLaughlin, , 1996McLaughlin and Wu, 1997;Zagon and McLaughlin, 1993). Endogenous opioids (Barron et al, 1995;Boluyt et al, 1993;Caffrey et al, 1994;Dumont and Lemaire, 1988;Dumont et al, 1990Dumont et al, , 1991Forman et al, 1989Forman et al, , 1994Howells et al, 1986;Hughes et al, 1977;Lang et al, 1983;Low et al, 1990;McLaughlin, 1996;Millington et al, 1993;Ng and Ng, 1990;Springhorn and Claycomb, 1992;Tang et al, 1982;Wegener and Krummins, 1994;Weihe et al, 1985;Zagon et al, 1986) and gene expression of opioid prohormones (Boluyt et al, 1993;Caffrey et al, 1994;Dumont et al, 1991;Howells et al, 1986;Forman and Bagasra, 1992;Kew and Kilpatrick, 1990;Low et al, 1990;McLaughlin, 1996;Ouellette and Brakier-Gingras, 1988;Ouellette et al, 1991;Rao and Howells, 1992;Claycomb, 1989, 1992;Ventura et al, 1993Ventura et al, , 1994…”