Effects of stress-related signal molecules on cells associated with muscle tissue.
OBJECTIVE
To elucidate the physiologic background that makes muscle hypertrophy, especially that due to strenuous exercise, often parallel to stress sensitivity and signs of acute phase immune response.


METHODS
We used an animal model: lines of mice with hypertrophied (H) and normally developed (N) hind leg muscles, six in each case. Functional and receptor tests on cells from digested muscle tissue were made and analyzed by microplate cytofluorimetry and flow cytometry.


RESULTS
Higher percentages of cells with a phagocyte marker (> 2-fold) and with opioid (about 1.3-fold) receptors were found, whereas the portion of glucocorticoid receptor-bearing cells tended to differ only among H and N. Naloxone, an opioid receptor antagonist, failed only in H to exert a suppressive effect on dihydrorhodamine 123 oxidation.


CONCLUSIONS
These results and differences in responses of lipid trafficking and proteolytic activities to cortisol, naloxone and adrenergic receptor agonists suggest that not only the cell population associated with muscle tissue but also receptor-mediated responses that are known to be related to stress coping are different between H and N.
Loehrke
B
B
Research Institute of Animal Biology Dummerstorf-Rostock, Germany.
Renne
U
U
Viergutz
T
T
Ender
K
K
Krüger
B
B
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D004837:Epinephrine / Q000494:pharmacology; D005434:Flow Cytometry; D005938:Glucocorticoids / Q000378:metabolism; D006614:Hindlimb / Q000737:chemistry / Q000187:drug effects; D006854:Hydrocortisone / Q000494:pharmacology; D006984:Hypertrophy / Q000378:metabolism; D050356:Lipid Metabolism; D008297:Male; D051379:Mice; D018482:Muscle, Skeletal / Q000737:chemistry* / Q000187:drug effects / Q000473:pathology; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists; D009294:Narcotics / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D010084:Oxidation-Reduction; D010586:Phagocytes / Q000378:metabolism; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic / Q000378:metabolism*; D018000:Receptors, Peptide / Q000378:metabolism*; D016897:Respiratory Burst / Q000187:drug effects; D012235:Rhodamines / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D005938:Glucocorticoids; D009292:Narcotic Antagonists; D009294:Narcotics; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic; D018000:Receptors, Peptide; D012235:Rhodamines; C058319:dihydrorhodamine 123; D009270:Naloxone; D013755:Tetradecanoylphorbol Acetate; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine